PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
22371793-10	2010	CONCLUSIONS: The present study indicates that CoQ improves the most important component of the antioxidant defence system - SOD-1, which is responsible for O(2) ( -) scavenging.	coq	46-49	superoxide dismutase 1	Homo sapiens	124-129
20635514-4	2010	In this study, a liposomal formulation composed of soybean phosphatidylcholine (SPC) and alpha-tocopherol (Vit E) was utilized to encapsulate CoQ10 for topical application.	coq	142-147	vitrin	Rattus norvegicus	107-110
20495296-7	2010	Colonic mucosa of DMH-injected rats had significantly greater COX-2 and iNOS gene expression than those of control rats, while treatment with CoQ10 induced an inhibitory effect on over-expression of COX-2 and iNOS in colon tumors.	coq	142-147	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	62-67
20495296-7	2010	Colonic mucosa of DMH-injected rats had significantly greater COX-2 and iNOS gene expression than those of control rats, while treatment with CoQ10 induced an inhibitory effect on over-expression of COX-2 and iNOS in colon tumors.	coq	142-147	nitric oxide synthase 2	Rattus norvegicus	72-76
20495296-7	2010	Colonic mucosa of DMH-injected rats had significantly greater COX-2 and iNOS gene expression than those of control rats, while treatment with CoQ10 induced an inhibitory effect on over-expression of COX-2 and iNOS in colon tumors.	coq	142-147	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	199-204
20495296-7	2010	Colonic mucosa of DMH-injected rats had significantly greater COX-2 and iNOS gene expression than those of control rats, while treatment with CoQ10 induced an inhibitory effect on over-expression of COX-2 and iNOS in colon tumors.	coq	142-147	nitric oxide synthase 2	Rattus norvegicus	209-213
20046059-5	2010	For example, SAMP1 line is used to study the anti-aging effect of the antioxidant containing foods and various anti-oxidants, such as coenzyme Q10, vitamin C, lycopene.	coq	134-146	transmembrane protein 201	Mus musculus	13-18
19478336-5	2009	The rate of superoxide generation by the reconstituted bc(1) complex increased exponentially with increased magnitude of the membrane potential, a finding that is compatible with the suggestion that membrane potential inhibits electron transfer from the cytochrome b(L) to b(H) hemes, thereby promoting the formation of a ubisemiquinone radical that interacts with oxygen to generate superoxide.	coq	322-344	cytochrome b	Saccharomyces cerevisiae S288C	254-266
19647758-11	2009	These results demonstrated that solubilized CoQ10 inhibited DMN-induced liver fibrosis through suppression of TGF-beta1 expression via Nrf2/ARE activation.	coq	44-49	transforming growth factor, beta 1	Mus musculus	110-119
19647758-11	2009	These results demonstrated that solubilized CoQ10 inhibited DMN-induced liver fibrosis through suppression of TGF-beta1 expression via Nrf2/ARE activation.	coq	44-49	nuclear factor, erythroid derived 2, like 2	Mus musculus	135-139
18817789-10	2008	Oral administration of Co Q10 in a low dose 200 mg/kg/day (group III) or a high dose 600 mg/kg/day (group IV), resulted in amelioration of the mitochondrial induced apoptosis by dose-dependent restoration of striatal complex I activity, ATP levels with temperate increase in expression of Bcl-2 as well as decrease in catalepsy score.	coq	23-29	BCL2, apoptosis regulator	Rattus norvegicus	289-294
18029098-4	2008	Using this system, we found that coenzyme Q(10) (CoQ(10)) can inhibit Cdt1-geminin interaction in vitro.	coq	49-52	chromatin licensing and DNA replication factor 1	Homo sapiens	70-74
19049556-1	2008	BACKGROUND AND PURPOSE: A pilot study of high dose coenzyme Q(10) (CoQ(10))/vitamin E therapy in Friedreich"s ataxia (FRDA) patients resulted in significant clinical improvements in most patients.	coq	67-74	frataxin	Homo sapiens	118-122
18230681-2	2008	Last year, we reported the first mutations in CoQ(10) biosynthetic genes, COQ2, which encodes 4-parahydroxybenzoate: polyprenyl transferase; and PDSS2, which encodes subunit 2 of decaprenyl diphosphate synthase.	coq	46-53	coenzyme Q2, polyprenyltransferase	Homo sapiens	74-78
18230681-2	2008	Last year, we reported the first mutations in CoQ(10) biosynthetic genes, COQ2, which encodes 4-parahydroxybenzoate: polyprenyl transferase; and PDSS2, which encodes subunit 2 of decaprenyl diphosphate synthase.	coq	46-53	decaprenyl diphosphate synthase subunit 2	Homo sapiens	145-150
18230681-2	2008	Last year, we reported the first mutations in CoQ(10) biosynthetic genes, COQ2, which encodes 4-parahydroxybenzoate: polyprenyl transferase; and PDSS2, which encodes subunit 2 of decaprenyl diphosphate synthase.	coq	46-53	decaprenyl diphosphate synthase subunit 2	Homo sapiens	166-210
18230681-6	2008	PDSS2 mutant fibroblasts have 12% CoQ(10) relative to control cells and markedly reduced ATP synthesis, but do not show increased reactive oxygen species (ROS) production, signs of oxidative stress, or increased antioxidant defense markers.	coq	34-37	decaprenyl diphosphate synthase subunit 2	Homo sapiens	0-5
18230681-7	2008	In contrast, COQ2 mutant fibroblasts have 30% CoQ(10) with partial defect in ATP synthesis, as well as significantly increased ROS production and oxidation of lipids and proteins.	coq	46-49	coenzyme Q2, polyprenyltransferase	Homo sapiens	13-17
18319074-8	2008	Three out of four patients tested showed a low endogenous pool of CoQ(10) in their fibroblasts or lymphoblasts, and two out of three patients showed impaired ubiquinone synthesis, strongly suggesting that ADCK3 is also involved in CoQ(10) biosynthesis.	coq	66-73	coenzyme Q8A	Homo sapiens	205-210
18319074-8	2008	Three out of four patients tested showed a low endogenous pool of CoQ(10) in their fibroblasts or lymphoblasts, and two out of three patients showed impaired ubiquinone synthesis, strongly suggesting that ADCK3 is also involved in CoQ(10) biosynthesis.	coq	231-238	coenzyme Q8A	Homo sapiens	205-210
18543930-10	2008	High performance liquid chromatographic (HPLC) analysis revealed that a substantial portion of CoQ9 had been converted into CoQ10.	coq	124-129	ubiquinone biosynthesis protein COQ9, mitochondrial	Cavia porcellus	95-99
18543930-11	2008	The results indicate that CoQ9 by itself, or after being converted into CoQ10, reduced myocardial ischemia/reperfusion-induced injury.	coq	72-77	ubiquinone biosynthesis protein COQ9, mitochondrial	Cavia porcellus	26-30
18787645-5	2008	Statin, 3-hydroxy-3- methyl-glutaryl (HMG)-CoA reductase inhibitor therapy inhibits conversion of HMG-CoA to mevalonate and lowers plasma CoQ(10) concentrations.	coq	138-141	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	8-56
18343482-7	2008	Since exogenous CoQ10 rescued the mitochondrial dysfunction and suppressed apoptosis in clk-1-deficient cells, we propose that clk-1-deficiency induces apoptosis associated with mitochondrial dysfunction due to a lack of CoQ, which may lead to embryonic lethality in mice around E10.5.	coq	16-21	CDC-like kinase 1	Mus musculus	88-93
18029098-4	2008	Using this system, we found that coenzyme Q(10) (CoQ(10)) can inhibit Cdt1-geminin interaction in vitro.	coq	49-52	geminin DNA replication inhibitor	Homo sapiens	75-82
18029098-6	2008	CoQ(10), having a longer isoprenoid chain, was the strongest inhibitor of Cdt1-geminin binding in the tested CoQs, with 50% inhibition observed at concentrations of 16.2 muM.	coq	0-3	chromatin licensing and DNA replication factor 1	Homo sapiens	74-78
18029098-6	2008	CoQ(10), having a longer isoprenoid chain, was the strongest inhibitor of Cdt1-geminin binding in the tested CoQs, with 50% inhibition observed at concentrations of 16.2 muM.	coq	0-3	geminin DNA replication inhibitor	Homo sapiens	79-86
18029098-9	2008	These results suggested that CoQ(10) inhibits Cdt1-geminin complex formation by binding to Cdt1 and thereby could liberate Cdt1 from inhibition by geminin.	coq	29-36	geminin DNA replication inhibitor	Homo sapiens	147-154
18029098-10	2008	Using three-dimensional computer modeling analysis, CoQ(10) was considered to interact with the geminin interaction interface on Cdt1, and was assumed to make hydrogen bonds with the residue of Arg243 of Cdt1.	coq	52-59	geminin DNA replication inhibitor	Homo sapiens	96-103
18029098-10	2008	Using three-dimensional computer modeling analysis, CoQ(10) was considered to interact with the geminin interaction interface on Cdt1, and was assumed to make hydrogen bonds with the residue of Arg243 of Cdt1.	coq	52-59	chromatin licensing and DNA replication factor 1	Homo sapiens	129-133
18029098-10	2008	Using three-dimensional computer modeling analysis, CoQ(10) was considered to interact with the geminin interaction interface on Cdt1, and was assumed to make hydrogen bonds with the residue of Arg243 of Cdt1.	coq	52-59	chromatin licensing and DNA replication factor 1	Homo sapiens	204-208
18029098-6	2008	CoQ(10), having a longer isoprenoid chain, was the strongest inhibitor of Cdt1-geminin binding in the tested CoQs, with 50% inhibition observed at concentrations of 16.2 muM.	coq	109-113	chromatin licensing and DNA replication factor 1	Homo sapiens	74-78
18029098-6	2008	CoQ(10), having a longer isoprenoid chain, was the strongest inhibitor of Cdt1-geminin binding in the tested CoQs, with 50% inhibition observed at concentrations of 16.2 muM.	coq	109-113	geminin DNA replication inhibitor	Homo sapiens	79-86
18029098-7	2008	Surface plasmon resonance analysis demonstrated that CoQ(10) bound selectively to Cdt1, but did not interact with geminin.	coq	53-60	chromatin licensing and DNA replication factor 1	Homo sapiens	82-86
18029098-9	2008	These results suggested that CoQ(10) inhibits Cdt1-geminin complex formation by binding to Cdt1 and thereby could liberate Cdt1 from inhibition by geminin.	coq	29-36	chromatin licensing and DNA replication factor 1	Homo sapiens	46-50
18029098-9	2008	These results suggested that CoQ(10) inhibits Cdt1-geminin complex formation by binding to Cdt1 and thereby could liberate Cdt1 from inhibition by geminin.	coq	29-36	geminin DNA replication inhibitor	Homo sapiens	51-58
18029098-9	2008	These results suggested that CoQ(10) inhibits Cdt1-geminin complex formation by binding to Cdt1 and thereby could liberate Cdt1 from inhibition by geminin.	coq	29-36	chromatin licensing and DNA replication factor 1	Homo sapiens	91-95
18029098-9	2008	These results suggested that CoQ(10) inhibits Cdt1-geminin complex formation by binding to Cdt1 and thereby could liberate Cdt1 from inhibition by geminin.	coq	29-36	chromatin licensing and DNA replication factor 1	Homo sapiens	91-95
15240412-3	2004	Moreover, a preserving potential of the antioxidant and bioenergetic coenzyme Q(10) (CoQ(10)) on the activities of tyrosine hydroxylase (TH), complexes I and II of the respiratory chain, and hexokinase activity in striatal slice cultures against MPP(+) is demonstrated.	coq	69-83	hexokinase 1	Homo sapiens	191-201
18181031-0	2008	Coenzyme Q10 attenuates beta-amyloid pathology in the aged transgenic mice with Alzheimer presenilin 1 mutation.	coq	0-12	presenilin 1	Mus musculus	90-102
18181031-3	2008	In our present study, we tested the effect of coenzyme Q10 (CoQ10), an endogenous antioxidant and a powerful free radical scavenger, on A beta in the aged transgenic mice overexpressing Alzheimer presenilin 1-L235P (leucine-to-proline mutation at codon 235, 16-17 months old).	coq	46-58	presenilin 1	Mus musculus	196-208
17412732-0	2007	The myopathic form of coenzyme Q10 deficiency is caused by mutations in the electron-transferring-flavoprotein dehydrogenase (ETFDH) gene.	coq	22-34	electron transfer flavoprotein dehydrogenase	Homo sapiens	76-124
17412732-0	2007	The myopathic form of coenzyme Q10 deficiency is caused by mutations in the electron-transferring-flavoprotein dehydrogenase (ETFDH) gene.	coq	22-34	electron transfer flavoprotein dehydrogenase	Homo sapiens	126-131
17412732-9	2007	All of our patients carried autosomal recessive mutations in ETFDH, suggesting that ETFDH deficiency leads to a secondary CoQ10 deficiency.	coq	122-127	electron transfer flavoprotein dehydrogenase	Homo sapiens	61-66
17186472-3	2006	The first defect in a CoQ(10) biosynthetic gene, COQ2, was identified in a child with encephalomyopathy and nephrotic syndrome and in a younger sibling with only nephropathy.	coq	22-29	coenzyme Q2, polyprenyltransferase	Homo sapiens	49-53
16647250-6	2006	CoQ10 resulted in a marked improvement in motor performance and grip strength, with a reduction in weight loss, brain atrophy, and huntingtin inclusions in treated R6/2 mice.	coq	0-5	huntingtin	Mus musculus	131-141
16647250-8	2006	Oral administration of CoQ10 elevated CoQ10 plasma levels and significantly increased brain levels of CoQ9, CoQ10, and ATP in R6/2 mice, while reducing 8-hydroxy-2-deoxyguanosine concentrations, a marker of oxidative damage.	coq	23-28	coenzyme Q9	Mus musculus	102-106
16243845-15	2005	We suggest that the damage to Co-I and Co-II shifts O*2- generation from the CoQ10 sites to more proximal sites, such as flavines, and makes it independent of the RBM functional state.	coq	77-82	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	30-34
16243845-15	2005	We suggest that the damage to Co-I and Co-II shifts O*2- generation from the CoQ10 sites to more proximal sites, such as flavines, and makes it independent of the RBM functional state.	coq	77-82	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	39-44
16873928-2	2005	Culturing HL-60 cells in the presence of p-aminobenzoate, a competitive inhibitor of polyprenyl-4-hydroxybenzoate transferase (Coq2p), produced a significant decrease of CoQ(10) levels without affecting cell viability.	coq	170-173	coenzyme Q2, polyprenyltransferase	Homo sapiens	127-132
16048353-3	2005	HMG-CoA reductase is also the first committed rate-limiting step for the synthesis of a range of other compounds including steroid hormones and ubidecarenone (ubiquinone), otherwise known as coenzyme Q(10) (CoQ(10)).	coq	144-157	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	0-17
17855635-3	2007	The COQ2 gene encodes the para-hydroxybenzoate-polyprenyl-transferase enzyme of the CoQ(10) synthesis pathway.	coq	84-91	coenzyme Q2, polyprenyltransferase	Homo sapiens	4-8
17644511-1	2007	AIMS: This randomized controlled study was designed to determine whether oral coenzyme Q(10) (CoQ(10)) supplementation (100 mg tid) was able to improve extracellular superoxide dismutase (ecSOD) activity and endothelium-dependent (ED) vasodilation in patients with coronary artery disease (CAD).	coq	94-101	superoxide dismutase 3	Homo sapiens	152-186
17644511-1	2007	AIMS: This randomized controlled study was designed to determine whether oral coenzyme Q(10) (CoQ(10)) supplementation (100 mg tid) was able to improve extracellular superoxide dismutase (ecSOD) activity and endothelium-dependent (ED) vasodilation in patients with coronary artery disease (CAD).	coq	94-101	superoxide dismutase 3	Homo sapiens	188-193
17644511-10	2007	In particular, improvements elicited by CoQ(10) supplementation were remarkable in subjects presenting low initial endothelium-bound ecSOD and thus more prone to oxidative stress.	coq	40-47	superoxide dismutase 3	Homo sapiens	133-138
17644511-11	2007	CONCLUSION: Improvements in the ED relaxation and endothelium-bound ecSOD activity might be related to CoQ(10) capability of enhancing endothelial functionality by counteracting nitric oxide oxidation.	coq	103-110	superoxide dismutase 3	Homo sapiens	68-73
16364609-8	2006	In addition, combined minocycline and CoQ10 treatment attenuated gross brain atrophy, striatal neuron atrophy, and huntingtin aggregation in the R6/2 mice relative to individual treatment.	coq	38-43	huntingtin	Mus musculus	115-125
16388100-5	2006	CoQ10 treatment also reduced lipid peroxidation and increased antioxidant parameters like superoxide dismutase, catalase, and glutathione in the liver homogenates of diabetic rats.	coq	0-5	catalase	Rattus norvegicus	112-120
16679553-2	2006	In this study we have determined the neuroprotective role of coenzyme Q(10) (CoQ(10)) in ironinduced apoptosis in cultured human dopaminergic (SK-N-SH) neurons, in metallothionein gene- manipulated mice, and in alpha-synuclein knockout (alpha-synko) mice with a primary objective to assess a possible therapeutic and anti-inflammatory potential for CoQ(10) in PD.	coq	61-74	synuclein, alpha	Mus musculus	211-226
16679553-2	2006	In this study we have determined the neuroprotective role of coenzyme Q(10) (CoQ(10)) in ironinduced apoptosis in cultured human dopaminergic (SK-N-SH) neurons, in metallothionein gene- manipulated mice, and in alpha-synuclein knockout (alpha-synko) mice with a primary objective to assess a possible therapeutic and anti-inflammatory potential for CoQ(10) in PD.	coq	77-83	synuclein, alpha	Mus musculus	211-226
16679553-7	2006	CoQ(10) treatment inhibited MPTP-induced NF-kappaB induction in all of the genotypes.	coq	0-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	41-50
15781239-3	2005	Using fluorescence spectroscopic analysis with thioflavin T and electron microscopic studies, we examined the effects of coenzyme Q(10) (CoQ(10)) on the formation, extension, and destabilization of fAbeta at pH 7.5 at 37 degrees C in vitro.	coq	137-140	FA complementation group B	Homo sapiens	198-204
15781239-5	2005	CoQ(10) dose-dependently inhibited fAbeta formation from amyloid beta-peptide (Abeta), as well as their extension.	coq	0-3	FA complementation group B	Homo sapiens	35-41
12732401-10	2003	Fenofibrate plus CoQ significantly improved (P<0.05) the AUC for ACh, BK and SNP without significantly altering basal responses to L-NMMA.	coq	17-20	kininogen 1	Homo sapiens	73-75
12885592-2	2003	Coenzyme Q(10) (CoQ(10)) in its reduced form, ubiquinol-10, effectively inhibits lipoprotein oxidation in vitro and in vivo; CoQ(10) supplements also inhibit atherosclerosis in apolipoprotein E gene knockout (apoE-/-) mice.	coq	16-19	apolipoprotein E	Mus musculus	177-193
12885592-2	2003	Coenzyme Q(10) (CoQ(10)) in its reduced form, ubiquinol-10, effectively inhibits lipoprotein oxidation in vitro and in vivo; CoQ(10) supplements also inhibit atherosclerosis in apolipoprotein E gene knockout (apoE-/-) mice.	coq	16-19	apolipoprotein E	Mus musculus	209-217
12885592-9	2003	Thus, like in apoE-/- mice, a high dose of supplemented CoQ(10) inhibits lipid oxidation in the artery wall of balloon-injured, hypercholesterolemic rabbits.	coq	56-59	apolipoprotein E	Mus musculus	14-18
11709071-6	2001	We conclude that CoQ acted in mitochondria through production of superoxide, which mediated uncoupling, probably by acting through uncoupling protein 2.	coq	17-20	uncoupling protein 2	Homo sapiens	131-151
11415943-10	2001	Thus, TNF-alpha induces mitochondrial ROS production in HUVEC that primarily occurs at the ubisemiquinone site and is mediated by ceramide-dependent signaling pathways involving CAPK.	coq	91-105	tumor necrosis factor	Homo sapiens	6-15
11304477-10	2001	Thus, in apoE-/- mice, VitE+CoQ(10) supplements are more antiatherogenic than CoQ(10) or VitE supplements alone and disease inhibition is associated with a decrease in aortic lipid hydroperoxides but not 7-ketocholesterol.	coq	28-35	apolipoprotein E	Mus musculus	9-13
10416029-6	1999	Also, CoQ10 addition decreased ceramide release after serum withdrawal by inhibition of magnesium-dependent plasma membrane neutral-sphingomyelinase.	coq	6-11	sphingomyelin phosphodiesterase 2	Homo sapiens	124-148
11136995-12	2000	Morphometrical studies demonstrated that CoQ(10) diminished neuronal injury in the hippocampal CA1, CA2 and CA3 zones.	coq	41-44	carbonic anhydrase 1	Rattus norvegicus	95-98
11136995-12	2000	Morphometrical studies demonstrated that CoQ(10) diminished neuronal injury in the hippocampal CA1, CA2 and CA3 zones.	coq	41-44	carbonic anhydrase 2	Rattus norvegicus	100-103
11136995-12	2000	Morphometrical studies demonstrated that CoQ(10) diminished neuronal injury in the hippocampal CA1, CA2 and CA3 zones.	coq	41-44	carbonic anhydrase 3	Rattus norvegicus	108-111
10416946-5	1999	Thus, it is proposed that correction of suboptimal CoQ status, by aiding the efficiency of G3PD and of respiratory chain function, will improve the glucose-stimulated insulin secretion of diabetic beta-cells.	coq	51-54	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	91-95
10416029-7	1999	Moreover, CoQ10 addition partially blocked activation of CPP32/caspase-3.	coq	10-15	caspase 3	Homo sapiens	57-62
10416029-7	1999	Moreover, CoQ10 addition partially blocked activation of CPP32/caspase-3.	coq	10-15	caspase 3	Homo sapiens	63-72
9852050-10	1998	The electron-leaking site is located at the reduced cytochrome b566 or ubisemiquinone of the Qo site because addition of MCLA to antimycin-treated cytochrome bc1 complex, in the presence of catalytic amounts of succinate-cytochrome c reductase, delayed cytochrome b reduction by succinate.	coq	71-85	cytochrome c, somatic	Homo sapiens	221-233
7819598-0	1994	Exogenous CoQ10 preserves plasma ubiquinone levels in patients treated with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.	coq	10-15	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	76-123
9833395-1	1998	The aim of the work was to evaluate the effect of CoQ10 (10 mg/kg body weight) on the morphological changes in the rat brain after the Et-1 induced cerebral ischemia.	coq	50-55	endothelin 1	Rattus norvegicus	135-139
9007665-11	1997	Inhibition of the platelet vitronectin receptor and a reduction of the platelet size are direct evidence of a link between dietary CoQ10 intake and platelets.	coq	131-136	vitronectin	Homo sapiens	27-38
9266502-5	1997	The reaction between DT-diaphorase and CoQ was also demonstrated in isolated rat liver hepatocytes in which incorporation of CoQ10 provided protection from adriamycin (adr)-induced mitochondrial membrane damage.	coq	125-130	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	21-34
9266502-6	1997	The role of DT-diaphorase in the antioxidant activity of CoQ was demonstrated by the co-incorporation of dicoumarol (dic), a potent inhibitor of DT-diaphorase, resulting in a loss of protection by incorporated CoQ10.	coq	210-215	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	12-25
9266532-7	1997	The CoQ10 and vitamin E showed some protection against toxic cell death and glutathione depletion caused by T-2 toxin.	coq	4-9	brachyury 2	Mus musculus	108-111
8903675-8	1996	It is proposed that ubiquinone-50 triggers the formation of hydroxyl radicals from 15-lipoxygenase-derived hydroperoxy-lipids via a Fenton-type reaction driven by ubisemiquinone radicals.	coq	163-177	arachidonate 15-lipoxygenase	Homo sapiens	83-98
7820130-2	1994	After the separation of oxidized and reduced CoQ homologues (CoQ8-CoQ10 and CoQ8H2-CoQ10H2) and alpha-TP on a reversed-phase column, oxidized CoQ homologues were reduced on a platinum catalyst reduction column, and then all the reduced forms were quantified with an electrochemical detector operated in the oxidation mode (+ 0.6 V vs. Ag/AgCl).	coq	45-48	coenzyme Q8A	Homo sapiens	61-65
1884524-5	1991	The CoQ10 level, studied so far in three DAT patients, was greatly reduced (approximately 50%) compared with controls.	coq	4-9	solute carrier family 6 member 3	Homo sapiens	41-44
1312087-13	1992	The different effects observed with the mitochondrial respiratory chain inhibitors provide suggestive evidence that mitochondrial production of oxygen radicals mainly generated at the ubisemiquinone site is a causal mechanism of TNF cytotoxicity.	coq	184-198	tumor necrosis factor	Mus musculus	229-232
1387460-8	1992	This study suggests that CoQ10, PGE1 and ONO-3708 protect liver damage by warm ischemia as results of improvement of metabolic disturbances of PGI2, TXA2, insulin and suppression of lipid peroxides production.	coq	25-30	insulin	Canis lupus familiaris	155-162
8241708-7	1993	Nevertheless, perfusion with exogenous CoQ10 maintains higher levels of endogenous CoQ9, and higher glutamate oxidation than in controls.	coq	39-44	coenzyme Q9	Rattus norvegicus	83-87
8241709-3	1993	However, the depressed beating rate and amplitude recovered almost completely within a few minutes by adding CoQ10 to the medium, and the effect of CoQ10 continued over 1 h. CoQ9 showed a cardiostimulatory effect similar to that of CoQ10, but CoQ8 and CoQ7 showed almost no effect.	coq	148-153	demethyl-Q 7	Mus musculus	252-256
8241709-3	1993	However, the depressed beating rate and amplitude recovered almost completely within a few minutes by adding CoQ10 to the medium, and the effect of CoQ10 continued over 1 h. CoQ9 showed a cardiostimulatory effect similar to that of CoQ10, but CoQ8 and CoQ7 showed almost no effect.	coq	148-153	demethyl-Q 7	Mus musculus	252-256
1309986-1	1992	A thenoyl trifluoroacetone-sensitive and antimycin-insensitive ubisemiquinone radical (Qs) is readily detected in purified succinate-cytochrome c reductase.	coq	63-85	cytochrome c, somatic	Homo sapiens	133-145
1720333-8	1991	Quinones may stimulate insulin release by mimicking physiologically-occurring quinones, such as CoQ10, by acting on the plasma membrane or in the cytosol.	coq	96-101	insulin	Homo sapiens	23-30
34798299-10	2022	Coenzyme Q10, which scavenges FA, was shown to ameliorate Abeta-induced AD pathological phenotypes, thus suggesting a causative relation between FA toxicity and AD.	coq	0-12	amyloid beta precursor protein	Homo sapiens	58-63
33799730-0	2021	CYP7A1, NPC1L1, ABCB1, and CD36 Polymorphisms Are Associated with Increased Serum Coenzyme Q10 after Long-Term Supplementation in Women.	coq	82-94	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	0-6
33799730-0	2021	CYP7A1, NPC1L1, ABCB1, and CD36 Polymorphisms Are Associated with Increased Serum Coenzyme Q10 after Long-Term Supplementation in Women.	coq	82-94	NPC1 like intracellular cholesterol transporter 1	Homo sapiens	8-14
33799730-6	2021	In addition, in women, rs3808607 (CYP7A1) and rs2072183 (NPC1L1) were significantly associated with a higher increase in CoQ10 per total cholesterol levels.	coq	121-126	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	34-40
33799730-6	2021	In addition, in women, rs3808607 (CYP7A1) and rs2072183 (NPC1L1) were significantly associated with a higher increase in CoQ10 per total cholesterol levels.	coq	121-126	NPC1 like intracellular cholesterol transporter 1	Homo sapiens	57-63
19834824-0	2010	Coenzyme Q10 reduces beta-amyloid plaque in an APP/PS1 transgenic mouse model of Alzheimer"s disease.	coq	0-12	presenilin 1	Mus musculus	51-54
33811899-0	2021	Chlorogenic acid, quercetin, coenzyme Q10 and silymarin modulate Keap1-Nrf2/heme oxygenase-1 signaling in thioacetamide-induced acute liver toxicity.	coq	29-41	Kelch-like ECH-associated protein 1	Rattus norvegicus	65-70
33811899-0	2021	Chlorogenic acid, quercetin, coenzyme Q10 and silymarin modulate Keap1-Nrf2/heme oxygenase-1 signaling in thioacetamide-induced acute liver toxicity.	coq	29-41	NFE2 like bZIP transcription factor 2	Rattus norvegicus	71-75
33811899-0	2021	Chlorogenic acid, quercetin, coenzyme Q10 and silymarin modulate Keap1-Nrf2/heme oxygenase-1 signaling in thioacetamide-induced acute liver toxicity.	coq	29-41	heme oxygenase 1	Rattus norvegicus	76-92
33811899-2	2021	We investigated the effect of chlorogenic acid (CGA), quercetin (Qt), coenzyme Q10 (Q10) and silymarin on the expression of Keap1/Nrf2 complex and its downstream target; heme oxygenase 1 (HO-1) as well as inflammation and apoptosis in an acute liver toxicity model induced by thioacetamide (TAA).	coq	70-82	Kelch-like ECH-associated protein 1	Rattus norvegicus	124-129
33811899-2	2021	We investigated the effect of chlorogenic acid (CGA), quercetin (Qt), coenzyme Q10 (Q10) and silymarin on the expression of Keap1/Nrf2 complex and its downstream target; heme oxygenase 1 (HO-1) as well as inflammation and apoptosis in an acute liver toxicity model induced by thioacetamide (TAA).	coq	70-82	NFE2 like bZIP transcription factor 2	Rattus norvegicus	130-134
33811899-2	2021	We investigated the effect of chlorogenic acid (CGA), quercetin (Qt), coenzyme Q10 (Q10) and silymarin on the expression of Keap1/Nrf2 complex and its downstream target; heme oxygenase 1 (HO-1) as well as inflammation and apoptosis in an acute liver toxicity model induced by thioacetamide (TAA).	coq	70-82	heme oxygenase 1	Rattus norvegicus	170-186
33811899-2	2021	We investigated the effect of chlorogenic acid (CGA), quercetin (Qt), coenzyme Q10 (Q10) and silymarin on the expression of Keap1/Nrf2 complex and its downstream target; heme oxygenase 1 (HO-1) as well as inflammation and apoptosis in an acute liver toxicity model induced by thioacetamide (TAA).	coq	79-82	Kelch-like ECH-associated protein 1	Rattus norvegicus	124-129
33811899-2	2021	We investigated the effect of chlorogenic acid (CGA), quercetin (Qt), coenzyme Q10 (Q10) and silymarin on the expression of Keap1/Nrf2 complex and its downstream target; heme oxygenase 1 (HO-1) as well as inflammation and apoptosis in an acute liver toxicity model induced by thioacetamide (TAA).	coq	79-82	NFE2 like bZIP transcription factor 2	Rattus norvegicus	130-134
34630650-7	2021	Pretreatment with CoQ10 prevented decreases in phosphorylated (p)-Akt, p-cAMP response element-binding protein, PGC-1alpha, NRF2 and mitochondrial transcription factor A, increasing mitochondrial biogenesis.	coq	18-23	thymoma viral proto-oncogene 1	Mus musculus	66-69
34664527-3	2022	RESULTS: The supplementation of CoQ10 decreased significantly the scores of Beck Depression Inventory (BDI) (p = .03) and Beck Anxiety Inventory (BAI) (p = .01) and high-sensitivity C-reactive protein (hs-CRP) level (p = .005) when comparing with the placebo group.	coq	32-37	C-reactive protein	Homo sapiens	182-200
34664527-4	2022	Moreover, CoQ10 group exhibited a significant drop in total testosterone (p = .004), dehydroepiandrosterone sulfate (DHEAS) (p < .001), hirsutism (p = .002) and malondialdehyde (MDA) (p = .001) levels in the serum, and a significant rise in sex hormone-binding globulin (SHBG) (p < .001) and total antioxidant capacity (TAC) (p < .001) levels in the serum than the placebo group.	coq	10-15	sex hormone binding globulin	Homo sapiens	241-269
34664527-4	2022	Moreover, CoQ10 group exhibited a significant drop in total testosterone (p = .004), dehydroepiandrosterone sulfate (DHEAS) (p < .001), hirsutism (p = .002) and malondialdehyde (MDA) (p = .001) levels in the serum, and a significant rise in sex hormone-binding globulin (SHBG) (p < .001) and total antioxidant capacity (TAC) (p < .001) levels in the serum than the placebo group.	coq	10-15	sex hormone binding globulin	Homo sapiens	271-275
34668565-8	2021	Moreover, CoQ10 increased MerTK+ macrophages accumulation in the APAP-overdose liver and inhibition of MerTK signaling partly abrogated the protective role of CoQ10 treatment on the hepatic necrosis.	coq	10-15	MER proto-oncogene tyrosine kinase	Mus musculus	26-31
34668565-8	2021	Moreover, CoQ10 increased MerTK+ macrophages accumulation in the APAP-overdose liver and inhibition of MerTK signaling partly abrogated the protective role of CoQ10 treatment on the hepatic necrosis.	coq	10-15	MER proto-oncogene tyrosine kinase	Mus musculus	103-108
34668565-8	2021	Moreover, CoQ10 increased MerTK+ macrophages accumulation in the APAP-overdose liver and inhibition of MerTK signaling partly abrogated the protective role of CoQ10 treatment on the hepatic necrosis.	coq	159-164	MER proto-oncogene tyrosine kinase	Mus musculus	26-31
34668565-8	2021	Moreover, CoQ10 increased MerTK+ macrophages accumulation in the APAP-overdose liver and inhibition of MerTK signaling partly abrogated the protective role of CoQ10 treatment on the hepatic necrosis.	coq	159-164	MER proto-oncogene tyrosine kinase	Mus musculus	103-108
34668565-10	2021	In addition, CoQ10 treatment increased hepatic PCNA and Cyclin D1 expression and promoted activation of the beta-catenin signaling in APAP-overdose mice.	coq	13-18	proliferating cell nuclear antigen	Mus musculus	47-51
34668565-10	2021	In addition, CoQ10 treatment increased hepatic PCNA and Cyclin D1 expression and promoted activation of the beta-catenin signaling in APAP-overdose mice.	coq	13-18	cyclin D1	Mus musculus	56-65
34668565-10	2021	In addition, CoQ10 treatment increased hepatic PCNA and Cyclin D1 expression and promoted activation of the beta-catenin signaling in APAP-overdose mice.	coq	13-18	catenin (cadherin associated protein), beta 1	Mus musculus	108-120
34939895-12	2021	Co-administration of CoQ10 resulted in significant improvement in the histopathological picture, with a significant decrease in caspase-3 and iNOS immunoexpression and downregulation of the Bax/Bcl-2 gene expression ratio.	coq	21-26	caspase 3	Rattus norvegicus	128-137
34939895-12	2021	Co-administration of CoQ10 resulted in significant improvement in the histopathological picture, with a significant decrease in caspase-3 and iNOS immunoexpression and downregulation of the Bax/Bcl-2 gene expression ratio.	coq	21-26	nitric oxide synthase 2	Rattus norvegicus	142-146
34939895-12	2021	Co-administration of CoQ10 resulted in significant improvement in the histopathological picture, with a significant decrease in caspase-3 and iNOS immunoexpression and downregulation of the Bax/Bcl-2 gene expression ratio.	coq	21-26	BCL2 associated X, apoptosis regulator	Rattus norvegicus	190-193
34939895-12	2021	Co-administration of CoQ10 resulted in significant improvement in the histopathological picture, with a significant decrease in caspase-3 and iNOS immunoexpression and downregulation of the Bax/Bcl-2 gene expression ratio.	coq	21-26	BCL2, apoptosis regulator	Rattus norvegicus	194-199
34408002-7	2021	Mechanistically, PDSS1, but not a catalytically inactive mutant, positively regulated the cellular level of coenzyme Q10 (CoQ10) and intracellular calcium levels, thereby inducing CAMK2A phosphorylation, which is essential for STAT3 phosphorylation in the cytoplasm.	coq	108-120	decaprenyl diphosphate synthase subunit 1	Homo sapiens	17-22
34408002-7	2021	Mechanistically, PDSS1, but not a catalytically inactive mutant, positively regulated the cellular level of coenzyme Q10 (CoQ10) and intracellular calcium levels, thereby inducing CAMK2A phosphorylation, which is essential for STAT3 phosphorylation in the cytoplasm.	coq	108-120	calcium/calmodulin dependent protein kinase II alpha	Homo sapiens	180-186
34408002-7	2021	Mechanistically, PDSS1, but not a catalytically inactive mutant, positively regulated the cellular level of coenzyme Q10 (CoQ10) and intracellular calcium levels, thereby inducing CAMK2A phosphorylation, which is essential for STAT3 phosphorylation in the cytoplasm.	coq	108-120	signal transducer and activator of transcription 3	Homo sapiens	227-232
34408002-7	2021	Mechanistically, PDSS1, but not a catalytically inactive mutant, positively regulated the cellular level of coenzyme Q10 (CoQ10) and intracellular calcium levels, thereby inducing CAMK2A phosphorylation, which is essential for STAT3 phosphorylation in the cytoplasm.	coq	122-127	decaprenyl diphosphate synthase subunit 1	Homo sapiens	17-22
34408002-7	2021	Mechanistically, PDSS1, but not a catalytically inactive mutant, positively regulated the cellular level of coenzyme Q10 (CoQ10) and intracellular calcium levels, thereby inducing CAMK2A phosphorylation, which is essential for STAT3 phosphorylation in the cytoplasm.	coq	122-127	calcium/calmodulin dependent protein kinase II alpha	Homo sapiens	180-186
34408002-7	2021	Mechanistically, PDSS1, but not a catalytically inactive mutant, positively regulated the cellular level of coenzyme Q10 (CoQ10) and intracellular calcium levels, thereby inducing CAMK2A phosphorylation, which is essential for STAT3 phosphorylation in the cytoplasm.	coq	122-127	signal transducer and activator of transcription 3	Homo sapiens	227-232
34489184-0	2021	L-carnitine and Co Q10 ameliorate potassium dichromate -induced acute brain injury in rats targeting AMPK/AKT/NF-kappabeta.	coq	16-22	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	101-105
34489184-0	2021	L-carnitine and Co Q10 ameliorate potassium dichromate -induced acute brain injury in rats targeting AMPK/AKT/NF-kappabeta.	coq	16-22	AKT serine/threonine kinase 1	Rattus norvegicus	106-109
34489184-4	2021	The study aimed to investigate the influence of administration of L-carnitine or/and Co Q10 as theraputic agents against potassium dichromate (PD)-induced brain injury via AMPK/AKT/NF-kappabeta signaling pathway.	coq	85-91	AKT serine/threonine kinase 1	Rattus norvegicus	177-180
34489184-8	2021	Treatment with L-carnitine + Co Q10 ameliorated cognitive impairment and oxidative stress, decreased the brain contents of inflammatory mediators; TNF-alpha, IL-6, and NF-kappabeta elevated AMPK and AKT, as compared to each drug.	coq	29-35	tumor necrosis factor	Rattus norvegicus	147-156
34489184-8	2021	Treatment with L-carnitine + Co Q10 ameliorated cognitive impairment and oxidative stress, decreased the brain contents of inflammatory mediators; TNF-alpha, IL-6, and NF-kappabeta elevated AMPK and AKT, as compared to each drug.	coq	29-35	interleukin 6	Rattus norvegicus	158-162
34489184-8	2021	Treatment with L-carnitine + Co Q10 ameliorated cognitive impairment and oxidative stress, decreased the brain contents of inflammatory mediators; TNF-alpha, IL-6, and NF-kappabeta elevated AMPK and AKT, as compared to each drug.	coq	29-35	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	190-194
34489184-8	2021	Treatment with L-carnitine + Co Q10 ameliorated cognitive impairment and oxidative stress, decreased the brain contents of inflammatory mediators; TNF-alpha, IL-6, and NF-kappabeta elevated AMPK and AKT, as compared to each drug.	coq	29-35	AKT serine/threonine kinase 1	Rattus norvegicus	199-202
34489184-10	2021	L-carnitine + Co Q10 play important role in AMPK/AKT/NF-kappabeta pathway that responsible for their antioxidant and anti-inflammatory effects against PD-induced brain injury in rats.	coq	14-20	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	44-48
34489184-10	2021	L-carnitine + Co Q10 play important role in AMPK/AKT/NF-kappabeta pathway that responsible for their antioxidant and anti-inflammatory effects against PD-induced brain injury in rats.	coq	14-20	AKT serine/threonine kinase 1	Rattus norvegicus	49-52
34630650-7	2021	Pretreatment with CoQ10 prevented decreases in phosphorylated (p)-Akt, p-cAMP response element-binding protein, PGC-1alpha, NRF2 and mitochondrial transcription factor A, increasing mitochondrial biogenesis.	coq	18-23	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	112-122
34630650-7	2021	Pretreatment with CoQ10 prevented decreases in phosphorylated (p)-Akt, p-cAMP response element-binding protein, PGC-1alpha, NRF2 and mitochondrial transcription factor A, increasing mitochondrial biogenesis.	coq	18-23	nuclear factor, erythroid derived 2, like 2	Mus musculus	124-128
34656997-1	2021	BACKGROUND: Human coenzyme Q4 (COQ4) is essential for coenzyme Q10 (CoQ10) biosynthesis.	coq	54-66	coenzyme Q4	Homo sapiens	18-29
34717624-11	2021	Additionally, biomass yield to glucose (Yb/glc) and CoQ10 synthesis can be promoted using fruAB mutation, and glk plays a key role in glucose metabolism.	coq	52-57	glucokinase	Rhodobacter sphaeroides 2.4.1	110-113
34705188-9	2022	The surprising results were achieved by raise in COQ10 level, which could regulate the overexpression of the AMPK gene in stressful conditions.	coq	49-54	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	109-113
34656997-1	2021	BACKGROUND: Human coenzyme Q4 (COQ4) is essential for coenzyme Q10 (CoQ10) biosynthesis.	coq	54-66	coenzyme Q4	Homo sapiens	31-35
34656997-1	2021	BACKGROUND: Human coenzyme Q4 (COQ4) is essential for coenzyme Q10 (CoQ10) biosynthesis.	coq	68-73	coenzyme Q4	Homo sapiens	18-29
34656997-1	2021	BACKGROUND: Human coenzyme Q4 (COQ4) is essential for coenzyme Q10 (CoQ10) biosynthesis.	coq	68-73	coenzyme Q4	Homo sapiens	31-35
34837681-11	2021	However, the expression of Bcl-2 significantly increased as a result of CoQ10 treatment.	coq	72-77	B cell leukemia/lymphoma 2	Mus musculus	27-32
34357552-0	2021	Neuroprotective effects of coenzyme Q10 in Parkinson"s model via a novel Q10/miR-149-5p/MMPs pathway.	coq	27-39	microRNA 149	Rattus norvegicus	77-84
34357552-12	2021	RT-qPCR analysis has represented upregulation and downregulation of miR-149-5p and MMP-2,9, respectively, after miR-mimic and CoQ10 treatment.	coq	126-131	matrix metallopeptidase 2	Rattus norvegicus	83-90
34357552-14	2021	Taking together miR-149 and CoQ10 has shown to have an impressive potential to prevent damage to dopaminergic neurons caused by 6-OHDA injection through reducing MMP-2,9, increased TH expression, and improved motor function.	coq	28-33	matrix metallopeptidase 2	Rattus norvegicus	162-169
34246922-9	2021	Furthermore, in cellular systems, n-3 PUFAs favored the synthesis of CoQ10 over CoQ9, thus altering the ratio between CoQ isoforms through a mechanism that involved downregulation of farnesyl diphosphate synthase activity.	coq	69-74	farnesyl diphosphate synthase	Homo sapiens	183-212
34368857-3	2021	In 2007, the molecular basis of SCCD was demonstrated to be associated with a tumor suppressor, UbiA prenyltransferase domain-containing 1 (UBIAD1), which was isolated from the bladder mucosa and demonstrated to be involved in vitamin K2 and CoQ10 biosynthesis.	coq	242-247	UbiA prenyltransferase domain containing 1	Homo sapiens	96-138
34368857-3	2021	In 2007, the molecular basis of SCCD was demonstrated to be associated with a tumor suppressor, UbiA prenyltransferase domain-containing 1 (UBIAD1), which was isolated from the bladder mucosa and demonstrated to be involved in vitamin K2 and CoQ10 biosynthesis.	coq	242-247	UbiA prenyltransferase domain containing 1	Homo sapiens	140-146
34471290-7	2021	The connection of HPDL to CoQ10 biosynthesis provides crucial insights into the mechanisms underlying recently described neurological diseases related to HPDL deficiencies1-4 and cancers with HPDL overexpression5.	coq	26-31	4-hydroxyphenylpyruvate dioxygenase like	Homo sapiens	18-22
34765390-1	2021	We report a detailed clinical examination in a patient with primary coenzyme Q10 deficiency caused by biallelic mutations in the PDSS1 gene who presented clinical features of mitochondrial encephalopathy associated with pulmonary hypertension, livedo reticularis and particularly, chronic distal phalangeal erythema.	coq	68-80	decaprenyl diphosphate synthase subunit 1	Homo sapiens	129-134
34765390-6	2021	This is the first reported patient with PDSS1 mutations presenting with 3-methyl-glutaconic aciduria and distal phalangeal erythema, expanding the phenotype of primary coenzyme Q10 deficiency.	coq	168-180	decaprenyl diphosphate synthase subunit 1	Homo sapiens	40-45
34574891-2	2021	Oxidative stress might play an important role in metabolic effects and as a regulator of seizure control, while coenzyme Q10 (CoQ10) could improve insulin sensitivity through antioxidant effects.	coq	112-124	insulin	Homo sapiens	147-154
34574891-2	2021	Oxidative stress might play an important role in metabolic effects and as a regulator of seizure control, while coenzyme Q10 (CoQ10) could improve insulin sensitivity through antioxidant effects.	coq	126-131	insulin	Homo sapiens	147-154
34574891-6	2021	Moreover, the serum CoQ10 level was significantly correlated with the seizure frequency (r = -0.412, p = 0.037) and insulin level (r = 0.409, p = 0.038).	coq	20-25	insulin	Homo sapiens	116-123
34574891-7	2021	Based on stratification by insulin resistance (HOMA-IR > 2.4), the subgroup analysis showed that patients with a greater HOMA-IR had higher CoQ10 levels and lower seizure frequency, and had a significantly worse quality of life.	coq	140-145	insulin	Homo sapiens	27-34
34429186-10	2022	Additionally, treatment with CoQ10 increased the expression of Bcl2 and Sirt1 in cumulus cells.	coq	29-34	B cell leukemia/lymphoma 2	Mus musculus	63-67
34429186-10	2022	Additionally, treatment with CoQ10 increased the expression of Bcl2 and Sirt1 in cumulus cells.	coq	29-34	sirtuin 1	Mus musculus	72-77
34146758-9	2021	CoQ10 levels were significantly and positively correlated with both ferritin and CRP levels.	coq	0-5	C-reactive protein	Homo sapiens	81-84
34471290-7	2021	The connection of HPDL to CoQ10 biosynthesis provides crucial insights into the mechanisms underlying recently described neurological diseases related to HPDL deficiencies1-4 and cancers with HPDL overexpression5.	coq	26-31	4-hydroxyphenylpyruvate dioxygenase like	Homo sapiens	192-196
34290862-7	2021	At the end of the study, CoQ10 administration caused a considerable reduction in the Malondialdehyde (MDA) and Interleukin 6 (IL-6) concentrations (P < 0 001), Glasgow Coma Score (GCS; P = 0 02), ICU and hospital length of stay and mechanical ventilation (MV) duration (P < 0 001).	coq	25-30	interleukin 6	Homo sapiens	111-124
34290862-7	2021	At the end of the study, CoQ10 administration caused a considerable reduction in the Malondialdehyde (MDA) and Interleukin 6 (IL-6) concentrations (P < 0 001), Glasgow Coma Score (GCS; P = 0 02), ICU and hospital length of stay and mechanical ventilation (MV) duration (P < 0 001).	coq	25-30	interleukin 6	Homo sapiens	126-130
34187945-3	2021	The results showed Dox treatment significantly induced GES-1 apoptosis, but preconditioning in GES-1 cells with VC or CoQ10 significantly inhibited the Dox-induced decrease and other harm effects, including the expression and of IkappaKbeta, IkappaBalpha, NF-kappaB/p65 and tumor necrosis factor (TNF-alpha) in GES-1 cells.	coq	118-123	NFKB inhibitor alpha	Rattus norvegicus	242-254
34187945-3	2021	The results showed Dox treatment significantly induced GES-1 apoptosis, but preconditioning in GES-1 cells with VC or CoQ10 significantly inhibited the Dox-induced decrease and other harm effects, including the expression and of IkappaKbeta, IkappaBalpha, NF-kappaB/p65 and tumor necrosis factor (TNF-alpha) in GES-1 cells.	coq	118-123	synaptotagmin 1	Rattus norvegicus	266-269
34187945-3	2021	The results showed Dox treatment significantly induced GES-1 apoptosis, but preconditioning in GES-1 cells with VC or CoQ10 significantly inhibited the Dox-induced decrease and other harm effects, including the expression and of IkappaKbeta, IkappaBalpha, NF-kappaB/p65 and tumor necrosis factor (TNF-alpha) in GES-1 cells.	coq	118-123	tumor necrosis factor-like	Rattus norvegicus	274-295
34187945-3	2021	The results showed Dox treatment significantly induced GES-1 apoptosis, but preconditioning in GES-1 cells with VC or CoQ10 significantly inhibited the Dox-induced decrease and other harm effects, including the expression and of IkappaKbeta, IkappaBalpha, NF-kappaB/p65 and tumor necrosis factor (TNF-alpha) in GES-1 cells.	coq	118-123	tumor necrosis factor	Rattus norvegicus	297-306
34187945-5	2021	CoQ10 and VC treatment inhibits Dox-induced gastric mucosal injury by inhibiting the activation of the IkKB/IkappaBalpha/NF-kappaB/p65/TNF-alpha pathway, promoting anti-inflammatory effects of gastric tissue and regulating the composition of the intestinal flora.	coq	0-5	NFKB inhibitor alpha	Rattus norvegicus	108-120
34187945-5	2021	CoQ10 and VC treatment inhibits Dox-induced gastric mucosal injury by inhibiting the activation of the IkKB/IkappaBalpha/NF-kappaB/p65/TNF-alpha pathway, promoting anti-inflammatory effects of gastric tissue and regulating the composition of the intestinal flora.	coq	0-5	synaptotagmin 1	Rattus norvegicus	131-134
34187945-5	2021	CoQ10 and VC treatment inhibits Dox-induced gastric mucosal injury by inhibiting the activation of the IkKB/IkappaBalpha/NF-kappaB/p65/TNF-alpha pathway, promoting anti-inflammatory effects of gastric tissue and regulating the composition of the intestinal flora.	coq	0-5	tumor necrosis factor	Rattus norvegicus	135-144
34280918-7	2021	Combined CoQ10 and AES pretreatment significantly reduced lung injury markers; 52.42% reduction in serum C-reactive protein (CRP), 53.69% in alkaline phosphatase (ALKP) and 60.26% in lactate dehydrogenase (LDH) activities versus 44.58, 37.38, and 48.6% in CoQ10 and 33.81, 34.43, and 39.29% in AES-pretreated groups, respectively.	coq	9-14	C-reactive protein	Rattus norvegicus	105-123
34400868-5	2021	Candesartan and CoQ10 as well as their combination suppressed gastrocnemius content of angiotensin II while they raised angiotensin-converting enzyme 2 (ACE2) activity, angiotensin (1-7) expression, and Mas receptor mRNA level.	coq	16-21	angiotensinogen	Rattus norvegicus	87-101
34400868-5	2021	Candesartan and CoQ10 as well as their combination suppressed gastrocnemius content of angiotensin II while they raised angiotensin-converting enzyme 2 (ACE2) activity, angiotensin (1-7) expression, and Mas receptor mRNA level.	coq	16-21	angiotensin I converting enzyme 2	Rattus norvegicus	120-151
34400868-5	2021	Candesartan and CoQ10 as well as their combination suppressed gastrocnemius content of angiotensin II while they raised angiotensin-converting enzyme 2 (ACE2) activity, angiotensin (1-7) expression, and Mas receptor mRNA level.	coq	16-21	angiotensin I converting enzyme 2	Rattus norvegicus	153-157
34400868-6	2021	Consequently, candesartan and/or CoQ10 reversed the oxidative stress and inflammatory changes that occurred following HLI/R as demonstrated by the rise of SOD activity and the decline of MDA, TNF-alpha, and IL-6 skeletal muscle content.	coq	33-38	tumor necrosis factor	Rattus norvegicus	192-201
34400868-6	2021	Consequently, candesartan and/or CoQ10 reversed the oxidative stress and inflammatory changes that occurred following HLI/R as demonstrated by the rise of SOD activity and the decline of MDA, TNF-alpha, and IL-6 skeletal muscle content.	coq	33-38	interleukin 6	Rattus norvegicus	207-211
34400868-7	2021	Additionally, candesartan and/or CoQ10 diminished gastrocnemius active caspase-3 level and phospho-p38 MAPK protein expression.	coq	33-38	caspase 3	Rattus norvegicus	71-80
34280918-7	2021	Combined CoQ10 and AES pretreatment significantly reduced lung injury markers; 52.42% reduction in serum C-reactive protein (CRP), 53.69% in alkaline phosphatase (ALKP) and 60.26% in lactate dehydrogenase (LDH) activities versus 44.58, 37.38, and 48.6% in CoQ10 and 33.81, 34.43, and 39.29% in AES-pretreated groups, respectively.	coq	9-14	C-reactive protein	Rattus norvegicus	125-128
34280918-13	2021	Our results showed for the first time that the enhanced anti-inflammatory effect of combined CoQ10 and AES pretreatment prevented LPS-induced ALI via suppression of NLRP-3 inflammasome through regulation of HMGB1/TLR4 signaling pathway and mitochondrial stabilization.	coq	93-98	NLR family, pyrin domain containing 3	Rattus norvegicus	165-171
34280918-13	2021	Our results showed for the first time that the enhanced anti-inflammatory effect of combined CoQ10 and AES pretreatment prevented LPS-induced ALI via suppression of NLRP-3 inflammasome through regulation of HMGB1/TLR4 signaling pathway and mitochondrial stabilization.	coq	93-98	high mobility group box 1	Rattus norvegicus	207-212
34280918-13	2021	Our results showed for the first time that the enhanced anti-inflammatory effect of combined CoQ10 and AES pretreatment prevented LPS-induced ALI via suppression of NLRP-3 inflammasome through regulation of HMGB1/TLR4 signaling pathway and mitochondrial stabilization.	coq	93-98	toll-like receptor 4	Rattus norvegicus	213-217
34978671-9	2022	Co-treatment with CoQ10 significantly attenuated DOX-induced behavioral alterations via improving AChE activity in the brain tissue of rats.	coq	18-23	acetylcholinesterase	Rattus norvegicus	98-102
35636077-0	2022	Coenzyme Q10 attenuates renal fibrosis by inhibiting RIP1-RIP3-MLKL-mediated necroinflammation via Wnt3alpha/beta-catenin/GSK-3beta signaling in unilateral ureteral obstruction.	coq	0-12	myosin phosphatase Rho interacting protein	Rattus norvegicus	58-62
35636077-0	2022	Coenzyme Q10 attenuates renal fibrosis by inhibiting RIP1-RIP3-MLKL-mediated necroinflammation via Wnt3alpha/beta-catenin/GSK-3beta signaling in unilateral ureteral obstruction.	coq	0-12	mixed lineage kinase domain like pseudokinase	Rattus norvegicus	63-67
35636077-0	2022	Coenzyme Q10 attenuates renal fibrosis by inhibiting RIP1-RIP3-MLKL-mediated necroinflammation via Wnt3alpha/beta-catenin/GSK-3beta signaling in unilateral ureteral obstruction.	coq	0-12	Wnt family member 3A	Rattus norvegicus	99-108
35636077-0	2022	Coenzyme Q10 attenuates renal fibrosis by inhibiting RIP1-RIP3-MLKL-mediated necroinflammation via Wnt3alpha/beta-catenin/GSK-3beta signaling in unilateral ureteral obstruction.	coq	0-12	catenin beta 1	Rattus norvegicus	109-121
35636077-0	2022	Coenzyme Q10 attenuates renal fibrosis by inhibiting RIP1-RIP3-MLKL-mediated necroinflammation via Wnt3alpha/beta-catenin/GSK-3beta signaling in unilateral ureteral obstruction.	coq	0-12	glycogen synthase kinase 3 alpha	Rattus norvegicus	122-131
35636077-4	2022	The influence of CoQ10 on renal injury caused by UUO was evaluated by histopathology and analysis of gene expression, oxidative stress, intracellular organelles, apoptosis, and Wnt3alpha/beta-catenin/GSK-3beta signaling H2O2-exposed human kidney (HK-2) cells were also examined after treatment with CoQ10 or an RIP inhibitor.	coq	17-22	glycogen synthase kinase 3 alpha	Homo sapiens	200-209
35636077-10	2022	CONCLUSION: These findings suggest that CoQ10 attenuates renal fibrosis by inhibiting RIP1-RIP3-MLKL-mediated necroinflammation via Wnt3alpha/beta-catenin/GSK-3beta signaling in UUO.	coq	40-45	myosin phosphatase Rho interacting protein	Rattus norvegicus	91-95
35636077-10	2022	CONCLUSION: These findings suggest that CoQ10 attenuates renal fibrosis by inhibiting RIP1-RIP3-MLKL-mediated necroinflammation via Wnt3alpha/beta-catenin/GSK-3beta signaling in UUO.	coq	40-45	mixed lineage kinase domain like pseudokinase	Rattus norvegicus	96-100
35636077-10	2022	CONCLUSION: These findings suggest that CoQ10 attenuates renal fibrosis by inhibiting RIP1-RIP3-MLKL-mediated necroinflammation via Wnt3alpha/beta-catenin/GSK-3beta signaling in UUO.	coq	40-45	Wnt family member 3A	Homo sapiens	132-141
35636077-10	2022	CONCLUSION: These findings suggest that CoQ10 attenuates renal fibrosis by inhibiting RIP1-RIP3-MLKL-mediated necroinflammation via Wnt3alpha/beta-catenin/GSK-3beta signaling in UUO.	coq	40-45	catenin beta 1	Homo sapiens	142-154
35636077-10	2022	CONCLUSION: These findings suggest that CoQ10 attenuates renal fibrosis by inhibiting RIP1-RIP3-MLKL-mediated necroinflammation via Wnt3alpha/beta-catenin/GSK-3beta signaling in UUO.	coq	40-45	glycogen synthase kinase 3 alpha	Homo sapiens	155-164
35212449-9	2022	The level of CoQ9 significantly increased in the liver, kidney, and plasma, while the level of CoQ10 significantly increased in most organ tissues in the CoQ10 + O2 group.	coq	154-159	coenzyme Q9	Rattus norvegicus	13-17
35585057-7	2022	Interestingly, while inhibition of FSP1 caused RPE cell death, which was aggravated by SIO exposure, overexpression of FSP1 effectively protected RPE cells from SIO-induced injury, accompanied by a significant down-regulation of CoQ10/NADH and lipid peroxidation.	coq	229-234	atlastin GTPase 1	Mus musculus	119-123
35143901-8	2022	Further treatment of UT-B-overexpressing B16 cells with reactive oxygen species scavenging agent N-acetyl-l-cysteine and coenzyme Q10 restored cell viability and mitochondrial function and increased polyamine production.	coq	121-133	solute carrier family 14 (urea transporter), member 1	Mus musculus	21-25
35453410-9	2022	Since the levels of coenzyme Q10 and muscle biomarkers, such as irisin and creatine kinase, are associated with sarcopenia, we suggest they could be used as candidate markers to assist in the diagnosis of sarcopenia.	coq	20-32	fibronectin type III domain containing 5	Homo sapiens	64-70
35379328-4	2022	UBIAD1, is a newly identified antioxidant enzyme that catalyzes coenzyme Q10 (CoQ10) and vitamin K2 biosynthesis in the Golgi apparatus membrane and mitochondria, respectively.	coq	64-76	UbiA prenyltransferase domain containing 1	Homo sapiens	0-6
35379328-4	2022	UBIAD1, is a newly identified antioxidant enzyme that catalyzes coenzyme Q10 (CoQ10) and vitamin K2 biosynthesis in the Golgi apparatus membrane and mitochondria, respectively.	coq	78-83	UbiA prenyltransferase domain containing 1	Homo sapiens	0-6
35239160-10	2022	CoQ10 prevented the increase in acetylcholinesterase activity, but not the decrease in the activity of Na+,K+-ATPase caused by QUIN.	coq	0-5	acetylcholinesterase	Rattus norvegicus	32-52
35239160-11	2022	We also observed that QUIN caused changes in the total ERK and phospho-Akt content, and these effects were partially prevented by CoQ10.	coq	130-135	Eph receptor B1	Rattus norvegicus	55-58
35239160-11	2022	We also observed that QUIN caused changes in the total ERK and phospho-Akt content, and these effects were partially prevented by CoQ10.	coq	130-135	AKT serine/threonine kinase 1	Rattus norvegicus	71-74
35633481-5	2022	The activation of the mitochondrial electron transport chain (ETC) by Coenzyme Q10 could rescue the promotion of DPSC senescence induced by the knockdown of IGFBP7, whereas the inhibition of ETC by rotenone attenuated the prevention of DPSC senescence induced by IGFBP7 overexpression.	coq	70-82	insulin like growth factor binding protein 7	Homo sapiens	157-163
35633481-5	2022	The activation of the mitochondrial electron transport chain (ETC) by Coenzyme Q10 could rescue the promotion of DPSC senescence induced by the knockdown of IGFBP7, whereas the inhibition of ETC by rotenone attenuated the prevention of DPSC senescence induced by IGFBP7 overexpression.	coq	70-82	insulin like growth factor binding protein 7	Homo sapiens	263-269
35233569-7	2022	Mito-MES reduced production of IL-6 by SARS-CoV-2 infected epithelial cells through its antioxidant properties (Nrf2 agonist, coenzyme Q 10 moiety) and the dTPP moiety.	coq	126-139	interleukin 6	Homo sapiens	31-35
35241098-6	2022	RESULTS: CoQ10 treatment significantly increased serum adiponectin levels at week 12 (165 (0, 362) ng/mL, p < 0.001) and at week 24 (523 (0, 1056) ng/mL, p < 0.001)), which was significant different compared with placebo (p < 0.001).	coq	9-14	adiponectin, C1Q and collagen domain containing	Homo sapiens	55-66
35241098-7	2022	The increase of adiponectin was negative associated with decrease in index of homeostasis model assessment of insulin resistance (HOMA-IR, r = - 0.465, p = 0.001), triglyceride (TG, r = - 0.297, p = 0.047), and low-density lipoprotein cholesterol (LDL-c, r = - 0.440, p = 0.002) at week 24 only in CoQ10-treated group.	coq	298-303	adiponectin, C1Q and collagen domain containing	Homo sapiens	16-27
35241098-13	2022	The beneficial effect of CoQ10 on glucolipid profile was mediated by adiponectin.	coq	25-30	adiponectin, C1Q and collagen domain containing	Homo sapiens	69-80
35063024-12	2022	Activation of ETC by Coenzyme Q10 (CoQ10) could restore the impaired osteogenic differentiation of hBMSCs by depletion of CB1 without or with TNF-alpha or INF-gamma stimulation.	coq	35-40	cannabinoid receptor 1	Homo sapiens	122-125
35296520-0	2022	Coenzyme Q10 deficiency can be expected to compromise Sirt1 activity.	coq	0-12	sirtuin 1	Homo sapiens	54-59
35296520-3	2022	Moreover, CoQ10 deficiency can be expected to decrease activities of Sirt1 and Sirt3 deacetylases, believed to be key determinants of health span.	coq	10-15	sirtuin 1	Homo sapiens	69-74
35296520-3	2022	Moreover, CoQ10 deficiency can be expected to decrease activities of Sirt1 and Sirt3 deacetylases, believed to be key determinants of health span.	coq	10-15	sirtuin 3	Homo sapiens	79-84
35296520-4	2022	Reduction of the cytoplasmic and mitochondrial NAD+/NADH ratio consequent to CoQ10 deficit can be expected to decrease the activity of these deacetylases by lessening availability of their obligate substrate NAD+ The increased oxidant production induced by CoQ10 deficiency can decrease the stability of Sirt1 protein by complementary mechanisms.	coq	77-82	sirtuin 1	Homo sapiens	304-309
35296520-6	2022	An analysis of the roles of Sirt1/Sirt3 in modulation of cellular function helps to rationalise clinical benefits of CoQ10 supplementation reported in heart failure, hypertension, non-alcoholic fatty liver disease, metabolic syndrome and periodontal disease.	coq	117-122	sirtuin 1	Homo sapiens	28-33
35296520-6	2022	An analysis of the roles of Sirt1/Sirt3 in modulation of cellular function helps to rationalise clinical benefits of CoQ10 supplementation reported in heart failure, hypertension, non-alcoholic fatty liver disease, metabolic syndrome and periodontal disease.	coq	117-122	sirtuin 3	Homo sapiens	34-39
35139868-1	2022	Coenzyme Q8A encodes the homologue of yeast coq8, an ATPase that is required for the biosynthesis of Coenzyme Q10, an essential component of the electron transport chain.	coq	101-113	protein kinase COQ8	Saccharomyces cerevisiae S288C	44-48
35111204-5	2021	Indeed, the death of our patients in early infancy indicates the pathogenicity of the p.Tyr83Ter and p.Gln461Ter variants and highlights the significance of the two variants for COQ6 enzyme function, which is necessary for the biosynthesis of coenzyme Q10.	coq	243-255	coenzyme Q6, monooxygenase	Homo sapiens	178-182
34978274-1	2022	We aimed to create a mechanical optic nerve damage model in rats and to investigate the neuroprotective effects of topical Coenzyme Q10 + Vitamin E TPGS (CoQ10+Vit E) molecule on retinal ganglion cells.	coq	123-135	vitrin	Rattus norvegicus	160-163
34978274-5	2022	Topical CoQ10 + Vit E TPGS solution was applied to the rats in the treatment group, one drop twice a day for 3 weeks.	coq	8-15	vitrin	Rattus norvegicus	16-19
3034247-0	1987	Stabilized ubisemiquinone in reconstituted succinate ubiquinone reductase.	coq	11-25	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	53-73
35154243-2	2021	In this review, we discuss the correlation of COQ4 genotypes, particularly the East Asian-specific c.370G > A variant, with the clinical presentations and therapeutic effectiveness of coenzyme Q10 supplementation from an exon-dependent perspective.	coq	184-196	coenzyme Q4	Homo sapiens	46-50
35154243-3	2021	Pathogenic COQ4 variants in exons 1-4 are associated with less life-threating presentations, late onset, responsiveness to CoQ10 therapy, and a relatively long lifespan.	coq	123-128	coenzyme Q4	Homo sapiens	11-15
35154243-4	2021	In contrast, pathogenic COQ4 variants in exons 5-7 are associated with early onset, unresponsiveness to CoQ10 therapy, and early death and are more fatal.	coq	104-109	coenzyme Q4	Homo sapiens	24-28
3034247-4	1987	A thenoyltrifluoroacetone sensitive free radical signal was detected by EPR spectroscopy in succinate-Q reductase reconstituted from this QP-S and SDH; the characteristics of this species identify it as ubisemiquinone.	coq	203-217	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	147-150
3009448-11	1986	One pathway allows the initial phase of cytochrome b reduction by a myxothiazol-sensitive reaction in which reduction of b by ubisemiquinone is linked to reduction of iron-sulfur protein and cytochrome c1 by ubiquinol.	coq	126-140	mitochondrially encoded cytochrome b	Homo sapiens	40-52
3941783-5	1986	CoQ therapy decreased CSF protein concentration and CSF lactate/pyruvate ratio.	coq	0-3	colony stimulating factor 2	Homo sapiens	22-25
3941783-5	1986	CoQ therapy decreased CSF protein concentration and CSF lactate/pyruvate ratio.	coq	0-3	colony stimulating factor 2	Homo sapiens	52-55
7074101-9	1982	(7) It is suggested that the need for ubiquinone for the oxidation of duroquinol is due to the requirement of ubisemiquinone for the oxidation of cytochrome b, duroquinol not being able to form a stabilized semiquinone.	coq	110-124	mitochondrially encoded cytochrome b	Homo sapiens	146-158
4063355-10	1985	It is concluded that CoQ-10 is incorporated into the membrane core, beyond C-2 of the PC acyl chains, with two bilayer curvature-dependent resonance positions.	coq	21-27	complement C2	Homo sapiens	75-78
4084344-6	1985	Pretreatment with coenzyme Q10 (E-0216, CoQ10), an antidetergent agent, prevented not only the development of mitochondrial dysfunction and the decrease in mitochondrial phospholipids but also the elevation of GOT, GPT, and mGOT although CoQ10 did not prevent the elevation of T-Bil and TBA levels.	coq	40-45	glutamic--pyruvic transaminase	Rattus norvegicus	215-218
6086391-0	1984	Localization of a ferricyanide-reactive site of cytochrome b-c1 complex, possibly of cytochrome b or ubisemiquinone, at the outer face of submitochondrial particles.	coq	101-115	mitochondrially encoded cytochrome b	Homo sapiens	48-60
7184359-0	1982	[Protective effect of CoQ 10 administration on cardial toxicity in FAC therapy].	coq	22-28	FA complementation group C	Homo sapiens	67-70
6288019-21	1982	Cytochrome b562 is postulated to be on the inner surface of the mitochondrial membrane and to bind either ubiquinone or ubisemiquinone, HQNO would bind to the reduced form of the cytochrome and colletotrichin to the oxidized form.	coq	120-134	mitochondrially encoded cytochrome b	Homo sapiens	0-12
7262508-2	1981	In the present study, experimental liver injury induced by CCl4 could be inhibited by Coenzyme Q10 (CoQ10) and in spite of exposure to CCl4 the liver tissue levels of thiobarbituric acid (TBA) reacting substances were not increased in rats pretreated with CoQ10.	coq	100-105	C-C motif chemokine ligand 4	Rattus norvegicus	59-63
6263261-7	1980	Thus the ubisemiquinone associated with succinate dehydrogenase (designated as SQS) functions mostly in the anionic form of the physiological pH range.	coq	9-23	farnesyl-diphosphate farnesyltransferase 1	Homo sapiens	79-82
34008150-10	2021	CONCLUSION: Overall, the findings showed that CoQ10 supplementation reduced some of the important markers of inflammation and MMPs in patients with breast cancer.	coq	46-51	matrix metallopeptidase 2	Homo sapiens	126-130
33999383-4	2022	METHODS: Searching the PubMed, EMBASE, and the Cochrane Library databases to identify randomized controlled trials investigating the effect of adding CoQ10 on creatine kinase (CK) activity and degree of muscle pain as two indicators of statin-induced myopathy.	coq	150-155	cytidine/uridine monophosphate kinase 1	Homo sapiens	159-174
33999383-8	2022	Compared with the controls, CK activity increased after adding CoQ10, but the change was not significant (mean difference, 3.29 U/L; 95% CI, - 29.58 to 36.17 U/L; P = 0.84).	coq	63-68	cytidine/uridine monophosphate kinase 1	Homo sapiens	28-30
33515676-8	2021	Oral administration of Coenzyme Q10, an essential co-factor known to meliorate mitochondrial oxidative stress and preserve bioenergetics, conferred a protection against AF attack in the mutant ALDH2*2 mice.	coq	23-35	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	193-198
33515676-10	2021	This inspired the development of a personalized therapeutic agent, Coenzyme Q10, to protect against AF attack in humans characterized by ALDH2*2 genotype.	coq	67-79	aldehyde dehydrogenase 2 family member	Homo sapiens	137-142
33411248-6	2021	Intake of N-acetylcysteine, coenzyme Q10 and melatonin is accompanied by increased Nrf2 activity.	coq	28-40	NFE2 like bZIP transcription factor 2	Homo sapiens	83-87
33859365-4	2022	RESULTS: CoQ10 promoted the expression of nuclear factor erythroid 2-related factor 2 and antioxidant enzymes.	coq	9-14	nuclear factor, erythroid derived 2, like 2	Mus musculus	42-85
33856607-0	2021	The protective role of Coenzyme Q10 in metallothionein-3 expression in liver and kidney upon rats" exposure to lead acetate.	coq	23-35	metallothionein 3	Rattus norvegicus	39-56
33856607-2	2021	In this study, we investigated the hepatic and renal expression of MT3 gene following exposure to lead acetate (PbAc) alone and PbAc plus CoQ10 as an adjuvant antioxidant.	coq	138-143	metallothionein 3	Rattus norvegicus	67-70
32572802-7	2021	There was also a significant improvement in TAC (p < 0.01 and p < 0.05) and SOD (p < 0.01 and p < 0.05) following treatment with CoQ10 and selenium respectively while CAT improved only with CoQ10 therapy (p < 0.05).	coq	129-134	superoxide dismutase 1	Homo sapiens	76-79
32572802-7	2021	There was also a significant improvement in TAC (p < 0.01 and p < 0.05) and SOD (p < 0.01 and p < 0.05) following treatment with CoQ10 and selenium respectively while CAT improved only with CoQ10 therapy (p < 0.05).	coq	129-134	catalase	Homo sapiens	167-170
32572802-7	2021	There was also a significant improvement in TAC (p < 0.01 and p < 0.05) and SOD (p < 0.01 and p < 0.05) following treatment with CoQ10 and selenium respectively while CAT improved only with CoQ10 therapy (p < 0.05).	coq	190-195	catalase	Homo sapiens	167-170
33393703-7	2021	Furthermore, EGCG + CoQ10 treatment inhibited CP-induced apoptosis by suppressing the activation and mitochondrial accumulation of proapoptotic proteins and preventing the inhibition of antiapoptotic protein expression, cytochrome c efflux, caspase-3 activation, and DNA fragmentation.	coq	20-25	caspase 3	Rattus norvegicus	241-250
33881976-0	2022	Coenzyme Q10 supplement rescues postovulatory oocyte aging by regulating SIRT4 expression.	coq	0-12	sirtuin 4	Homo sapiens	73-78
33881976-10	2022	Furthermore, SIRT4, which was first found to be up-regulated in postovulatory aged oocytes, decreased following CoQ10 treatment.	coq	112-117	sirtuin 4	Homo sapiens	13-18
33881396-1	2021	OBJECTIVE: ADCK3-related disease is a mitochondrial disorder associated with an abnormality of coenzyme Q10 metabolism.	coq	95-107	coenzyme Q8A	Homo sapiens	11-16
33548410-7	2021	Taurine and COQ-10 or their combination increased spermatogenesis, testicular 3ss-HSD, 17ss-HSD, G6PDH and LDH-X enzymes of naive and chlorpromazine-treated rats.	coq	12-18	glucose-6-phosphate dehydrogenase	Rattus norvegicus	97-102
33548410-7	2021	Taurine and COQ-10 or their combination increased spermatogenesis, testicular 3ss-HSD, 17ss-HSD, G6PDH and LDH-X enzymes of naive and chlorpromazine-treated rats.	coq	12-18	lactate dehydrogenase C	Rattus norvegicus	107-112
33782820-6	2022	Regarding oxidative stress and inflammation, pooled analysis showed that CoQ10 supplementation significantly reduced malonaldehyde (WMD: - 1.15 95% CI - 1.48 to - 0.81) and high-sensitivity C reactive protein levels (WMD: - 1.18 95% CI - 2.21 to - 0.15).	coq	73-78	C-reactive protein	Homo sapiens	190-208
33754447-0	2021	Coenzyme Q10 inhibits RANKL-induced osteoclastogenesis by regulation of mitochondrial apoptosis and oxidative stress in RAW264.7 cells.	coq	0-12	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	22-27
33754447-2	2021	We aimed to investigate the effects of CoQ10 on receptor activator of NF-kappaB ligand (RANKL)-induced osteoclastogenesis and the underlying molecular mechanisms.	coq	39-44	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	88-93
33754447-9	2021	Mechanically, CoQ10 statistically decreased the levels of Bcl-2 and cytochrome C in mitochondria and upregulated the levels of Bax, cleaved caspase 3, and cytochrome C in the cytoplasm.	coq	14-19	B cell leukemia/lymphoma 2	Mus musculus	58-63
33754447-9	2021	Mechanically, CoQ10 statistically decreased the levels of Bcl-2 and cytochrome C in mitochondria and upregulated the levels of Bax, cleaved caspase 3, and cytochrome C in the cytoplasm.	coq	14-19	BCL2-associated X protein	Mus musculus	127-130
33754447-9	2021	Mechanically, CoQ10 statistically decreased the levels of Bcl-2 and cytochrome C in mitochondria and upregulated the levels of Bax, cleaved caspase 3, and cytochrome C in the cytoplasm.	coq	14-19	caspase 3	Mus musculus	140-149
33754447-10	2021	Moreover, CoQ10 significantly decreased RANKL-induced osteoclastogenesis regardless of exposure to H2 O2 .	coq	10-15	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	40-45
33754447-11	2021	In addition, CoQ10 statistically reduced MDA activity and elevated the activities of SOD and CAT, as well as the expression of oxidative stress-related proteins.	coq	13-18	catalase	Mus musculus	93-96
33754447-12	2021	CoQ10 may inhibit RANKL-induced osteoclastogenesis by regulation of mitochondrial apoptosis and oxidative stress in RAW264.7 cells.	coq	0-5	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	18-23
33859365-12	2022	CoQ10 promoted the expression of Nrf2 and antioxidant enzymes.	coq	0-5	nuclear factor, erythroid derived 2, like 2	Mus musculus	33-37
33743807-4	2021	In the present study, we determined that the CoQ10-induced anti-allergic effects were mediated by up-regulation of Nrf2.	coq	45-50	NFE2 like bZIP transcription factor 2	Homo sapiens	115-119
33743807-11	2021	RESULTS: Co-Q10 with two supplementation (Mg-S and O-3) modulate MRC, BALf eosinophils, eosinophilic inflammation related genes (eotaxin, CCL11 and CCL24), peribronchial and perivascular inflammation, EPO, type 2 cytokines (IL-4, 5 and 13), IgE, histamine, Cyc-LT and LTB4 as main allergic bio-factors.	coq	9-15	C-C motif chemokine ligand 11	Homo sapiens	129-136
33743807-11	2021	RESULTS: Co-Q10 with two supplementation (Mg-S and O-3) modulate MRC, BALf eosinophils, eosinophilic inflammation related genes (eotaxin, CCL11 and CCL24), peribronchial and perivascular inflammation, EPO, type 2 cytokines (IL-4, 5 and 13), IgE, histamine, Cyc-LT and LTB4 as main allergic bio-factors.	coq	9-15	C-C motif chemokine ligand 11	Homo sapiens	138-143
33743807-11	2021	RESULTS: Co-Q10 with two supplementation (Mg-S and O-3) modulate MRC, BALf eosinophils, eosinophilic inflammation related genes (eotaxin, CCL11 and CCL24), peribronchial and perivascular inflammation, EPO, type 2 cytokines (IL-4, 5 and 13), IgE, histamine, Cyc-LT and LTB4 as main allergic bio-factors.	coq	9-15	C-C motif chemokine ligand 24	Homo sapiens	148-153
33743807-11	2021	RESULTS: Co-Q10 with two supplementation (Mg-S and O-3) modulate MRC, BALf eosinophils, eosinophilic inflammation related genes (eotaxin, CCL11 and CCL24), peribronchial and perivascular inflammation, EPO, type 2 cytokines (IL-4, 5 and 13), IgE, histamine, Cyc-LT and LTB4 as main allergic bio-factors.	coq	9-15	erythropoietin	Homo sapiens	201-204
33743807-11	2021	RESULTS: Co-Q10 with two supplementation (Mg-S and O-3) modulate MRC, BALf eosinophils, eosinophilic inflammation related genes (eotaxin, CCL11 and CCL24), peribronchial and perivascular inflammation, EPO, type 2 cytokines (IL-4, 5 and 13), IgE, histamine, Cyc-LT and LTB4 as main allergic bio-factors.	coq	9-15	interleukin 4	Homo sapiens	224-238
33743807-12	2021	Importantly, Co-Q10 treatment increased Nrf2 expression and Nrf2 induced antioxidant genes, glutathione redox and inhibited inflammation, oxidative stress injury, Th2 cytokines production and attenuated allergic inflammatory responses.	coq	13-19	NFE2 like bZIP transcription factor 2	Homo sapiens	40-44
33743807-12	2021	Importantly, Co-Q10 treatment increased Nrf2 expression and Nrf2 induced antioxidant genes, glutathione redox and inhibited inflammation, oxidative stress injury, Th2 cytokines production and attenuated allergic inflammatory responses.	coq	13-19	NFE2 like bZIP transcription factor 2	Homo sapiens	60-64
33743807-14	2021	Co-Q10 increases the Nrf2 expression and the Nrf2 over-expression has strong effect in control of type2 cytokines, allergic mediators and inflammatory factors that lead to harnessing of allergy and asthma.	coq	0-6	NFE2 like bZIP transcription factor 2	Homo sapiens	21-25
33743807-14	2021	Co-Q10 increases the Nrf2 expression and the Nrf2 over-expression has strong effect in control of type2 cytokines, allergic mediators and inflammatory factors that lead to harnessing of allergy and asthma.	coq	0-6	NFE2 like bZIP transcription factor 2	Homo sapiens	45-49
33080111-3	2021	To prevent respiratory poisoning, a dedicated set of enzymes comprising the mitochondrial sulfide oxidation pathway exists to clear H 2 S. The committed step in this pathway is catalyzed by sulfide quinone oxidoreductase (SQOR), which couples sulfide oxidation to coenzyme Q 10 reduction in the electron transport chain.	coq	264-277	crystallin zeta	Homo sapiens	198-220
33080111-3	2021	To prevent respiratory poisoning, a dedicated set of enzymes comprising the mitochondrial sulfide oxidation pathway exists to clear H 2 S. The committed step in this pathway is catalyzed by sulfide quinone oxidoreductase (SQOR), which couples sulfide oxidation to coenzyme Q 10 reduction in the electron transport chain.	coq	264-277	sulfide quinone oxidoreductase	Homo sapiens	222-226
33704555-1	2021	COQ4 is a component of an enzyme complex involved in the biosynthesis of coenzyme Q10 (CoQ10), a molecule with primary importance in cell metabolism.	coq	73-85	coenzyme Q4	Homo sapiens	0-4
33704555-1	2021	COQ4 is a component of an enzyme complex involved in the biosynthesis of coenzyme Q10 (CoQ10), a molecule with primary importance in cell metabolism.	coq	87-92	coenzyme Q4	Homo sapiens	0-4
33368479-8	2021	In addition, a decrease in the expression of caspase3 and caspase 8 was viewed in coenzyme Q10-treated groups.	coq	82-94	caspase 3	Rattus norvegicus	45-53
33368479-8	2021	In addition, a decrease in the expression of caspase3 and caspase 8 was viewed in coenzyme Q10-treated groups.	coq	82-94	caspase 8	Rattus norvegicus	58-67
32898935-3	2021	We report that the competitive coq2 inhibitor 4-nitrobenzoate (4-NB) decreased the cellular CoQ content and caused severe impairment of mitochondrial function in the T67 human glioma cell line.	coq	92-95	coenzyme Q2, polyprenyltransferase	Homo sapiens	31-35
32898935-7	2021	Exogenous CoQ supplementation partially recovered cholesterol content, HIF-1alpha degradation and ROS production, whereas only weakly improved the bioenergetic impairment induced by the CoQ depletion.	coq	10-13	hypoxia inducible factor 1 subunit alpha	Homo sapiens	71-81
33482334-2	2021	CoQ10 biosynthesis decreases with age in different tissues including skin and its biosynthesis can be modulated by 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors such as statins.	coq	0-5	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	155-173
33279678-1	2021	Multiple acyl-coenzyme A dehydrogenase deficiency (MADD), or glutaric aciduria type II (GAII), is a group of clinically heterogeneous disorders caused by mutations in electron transfer flavoprotein (ETF) and ETF-ubiquinone oxidoreductase (ETFQO) - the two enzymes responsible for the re-oxidation of enzyme-bound flavin adenine dinucleotide (FADH2) via electron transfer to the respiratory chain at the level of coenzyme Q10.	coq	412-424	MAP kinase activating death domain	Homo sapiens	51-55
33418245-0	2021	Coenzyme Q10 attenuates inflammation and fibrosis implicated in radiation enteropathy through suppression of NF-kB/TGF-beta/MMP-9 pathways.	coq	0-12	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	109-114
33418245-0	2021	Coenzyme Q10 attenuates inflammation and fibrosis implicated in radiation enteropathy through suppression of NF-kB/TGF-beta/MMP-9 pathways.	coq	0-12	transforming growth factor alpha	Homo sapiens	115-123
33418245-0	2021	Coenzyme Q10 attenuates inflammation and fibrosis implicated in radiation enteropathy through suppression of NF-kB/TGF-beta/MMP-9 pathways.	coq	0-12	matrix metallopeptidase 9	Homo sapiens	124-129
33418245-7	2021	CoQ10 attenuated radiation-induced oxidative stress by decreasing lipid peroxidation and increasing the antioxidant enzyme catalase activity and reduced glutathione level.	coq	0-5	catalase	Homo sapiens	123-131
33418245-8	2021	CoQ10 also counteracts inflammatory response mediated after radiation exposure through downregulating intestinal NF-kB expression which subsequently decreased the level of inflammatory cytokine IL-6 and the expression of COX-2.	coq	0-5	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	113-118
33418245-8	2021	CoQ10 also counteracts inflammatory response mediated after radiation exposure through downregulating intestinal NF-kB expression which subsequently decreased the level of inflammatory cytokine IL-6 and the expression of COX-2.	coq	0-5	interleukin 6	Homo sapiens	194-198
33418245-8	2021	CoQ10 also counteracts inflammatory response mediated after radiation exposure through downregulating intestinal NF-kB expression which subsequently decreased the level of inflammatory cytokine IL-6 and the expression of COX-2.	coq	0-5	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	221-226
33418245-10	2021	Therefore, CoQ10 is a promising radioprotector that could prevent intestinal complications and enhance the therapeutic ratio of radiotherapy in patients with pelvic tumors through suppressing the NF-kB/TGF-beta1/MMP-9 signaling pathway.	coq	11-16	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	196-201
33418245-10	2021	Therefore, CoQ10 is a promising radioprotector that could prevent intestinal complications and enhance the therapeutic ratio of radiotherapy in patients with pelvic tumors through suppressing the NF-kB/TGF-beta1/MMP-9 signaling pathway.	coq	11-16	transforming growth factor beta 1	Homo sapiens	202-211
33418245-10	2021	Therefore, CoQ10 is a promising radioprotector that could prevent intestinal complications and enhance the therapeutic ratio of radiotherapy in patients with pelvic tumors through suppressing the NF-kB/TGF-beta1/MMP-9 signaling pathway.	coq	11-16	matrix metallopeptidase 9	Homo sapiens	212-217
32830305-1	2021	The spectrum of coenzyme Q10 (CoQ10) deficiency syndromes comprises a variety of disorders, including a form of autosomal recessive cerebellar ataxia (ARCA2) caused by mutations in the AarF domain-containing kinase 3 gene (ADCK3).	coq	16-28	coenzyme Q8A	Homo sapiens	151-156
32830305-1	2021	The spectrum of coenzyme Q10 (CoQ10) deficiency syndromes comprises a variety of disorders, including a form of autosomal recessive cerebellar ataxia (ARCA2) caused by mutations in the AarF domain-containing kinase 3 gene (ADCK3).	coq	16-28	coenzyme Q8A	Homo sapiens	185-216
32830305-1	2021	The spectrum of coenzyme Q10 (CoQ10) deficiency syndromes comprises a variety of disorders, including a form of autosomal recessive cerebellar ataxia (ARCA2) caused by mutations in the AarF domain-containing kinase 3 gene (ADCK3).	coq	16-28	coenzyme Q8A	Homo sapiens	223-228
32830305-1	2021	The spectrum of coenzyme Q10 (CoQ10) deficiency syndromes comprises a variety of disorders, including a form of autosomal recessive cerebellar ataxia (ARCA2) caused by mutations in the AarF domain-containing kinase 3 gene (ADCK3).	coq	30-35	coenzyme Q8A	Homo sapiens	151-156
32830305-1	2021	The spectrum of coenzyme Q10 (CoQ10) deficiency syndromes comprises a variety of disorders, including a form of autosomal recessive cerebellar ataxia (ARCA2) caused by mutations in the AarF domain-containing kinase 3 gene (ADCK3).	coq	30-35	coenzyme Q8A	Homo sapiens	185-216
32830305-1	2021	The spectrum of coenzyme Q10 (CoQ10) deficiency syndromes comprises a variety of disorders, including a form of autosomal recessive cerebellar ataxia (ARCA2) caused by mutations in the AarF domain-containing kinase 3 gene (ADCK3).	coq	30-35	coenzyme Q8A	Homo sapiens	223-228
33630121-9	2021	While induction of CIN did not affect the renal levels of catalase, glutathione peroxidase (GPx), and thiobarbituric acid reactive substances, pretreatment of animals with CoQ10/NAC showed significant increase in GPx and catalase levels versus controls.	coq	172-177	catalase	Rattus norvegicus	221-229
33617219-4	2021	In the present study, CoQ10 is encapsulated into two milk derived proteins beta-lactoglobulin and lactoferrin (BLG and LF) to produce self-assembled nanostructures of around 100-300 nm with high encapsulation efficiency (5-10% w/w).	coq	22-27	lactotransferrin	Mus musculus	98-109
33620550-2	2021	This trial was, therefore, designed to determine CoQ10 efficacy on inflammation and antioxidant status, antimicrobial peptides, and microRNA-146a expression in UC patients.	coq	49-54	microRNA 146a	Homo sapiens	132-145
33620550-6	2021	Furthermore, CoQ10 remarkably increased serum levels of cathelicidin LL-37.	coq	13-18	cathelicidin antimicrobial peptide	Homo sapiens	69-74
33285023-5	2021	The visual system seems to be mainly involved when the first steps of CoQ10 synthesis are impaired (PDSS1, PDSS2, and COQ2 deficiency).	coq	70-75	decaprenyl diphosphate synthase subunit 1	Homo sapiens	100-105
33441012-0	2021	Coenzyme Q10 in COPD: An Unexplored Opportunity?	coq	0-12	COPD	Homo sapiens	16-20
33441012-3	2021	Even though oxidative stress and mitochondrial dysfunction is a well-studied phenomenon in COPD and there is a variety of studies that aim to counteract its effect, there is limited data available on the use of coenzyme Q10 in COPD.	coq	211-223	COPD	Homo sapiens	227-231
33441012-4	2021	The aim of the current review is to analyze the current data on the use of coenzyme Q10 in the management of COPD and frequently encountered comorbidities.	coq	75-87	COPD	Homo sapiens	109-113
33579045-3	2021	In a pre-clinical swine model of ischemic heart disease, we showed that daily administration of ubiquinone (coenzyme Q10, CoQ10) enhances the antioxidant status of mitochondria within chronically ischemic heart tissue, potentially via a PGC1alpha-dependent mechanism.	coq	108-120	PPARG coactivator 1 alpha	Sus scrofa	237-246
33579045-3	2021	In a pre-clinical swine model of ischemic heart disease, we showed that daily administration of ubiquinone (coenzyme Q10, CoQ10) enhances the antioxidant status of mitochondria within chronically ischemic heart tissue, potentially via a PGC1alpha-dependent mechanism.	coq	122-127	PPARG coactivator 1 alpha	Sus scrofa	237-246
33579045-4	2021	In a randomized controlled trial, among high-risk patients undergoing elective vascular surgery, we showed that NT Pro-BNP levels are an important means of risk-stratification during the perioperative period and can be lowered with administration of CoQ10 (400 mg/day) for 3 days prior to surgery.	coq	250-255	natriuretic peptide B	Homo sapiens	119-122
33413146-0	2021	Urinary coenzyme Q10 as a diagnostic biomarker and predictor of remission in a patient with ADCK4-associated Glomerulopathy: a case report.	coq	8-20	coenzyme Q8B	Homo sapiens	92-97
33413146-1	2021	BACKGROUND: AarF domain-containing kinase 4 (ADCK4)-associated glomerulopathy is a mitochondrial nephropathy caused by mutations in the ADCK4 gene, which disrupt coenzyme Q10 biosynthesis.	coq	162-174	coenzyme Q8B	Homo sapiens	12-43
33413146-1	2021	BACKGROUND: AarF domain-containing kinase 4 (ADCK4)-associated glomerulopathy is a mitochondrial nephropathy caused by mutations in the ADCK4 gene, which disrupt coenzyme Q10 biosynthesis.	coq	162-174	coenzyme Q8B	Homo sapiens	45-50
33413146-1	2021	BACKGROUND: AarF domain-containing kinase 4 (ADCK4)-associated glomerulopathy is a mitochondrial nephropathy caused by mutations in the ADCK4 gene, which disrupt coenzyme Q10 biosynthesis.	coq	162-174	coenzyme Q8B	Homo sapiens	136-141
33413146-7	2021	CONCLUSIONS: Although the use of urinary coenzyme Q10 as a diagnostic biomarker and predictor of clinical remission in patients with ADCK4-associated glomerulopathy should be confirmed by larger studies, we recommend measuring urinary coenzyme Q10 in patients with isolated proteinuria of unknown cause, since it may provide a diagnostic clue to mitochondrial nephropathy.	coq	41-53	coenzyme Q8B	Homo sapiens	133-138
33285023-5	2021	The visual system seems to be mainly involved when the first steps of CoQ10 synthesis are impaired (PDSS1, PDSS2, and COQ2 deficiency).	coq	70-75	coenzyme Q2, polyprenyltransferase	Homo sapiens	118-122
32544011-4	2021	In addition, supplementation with CoQ10 resulted in a significant reduction in serum VCAM-1 (p = .002) and E-selectin (p = .006) compared with the control group.	coq	34-39	vascular cell adhesion molecule 1	Homo sapiens	85-91
32544011-4	2021	In addition, supplementation with CoQ10 resulted in a significant reduction in serum VCAM-1 (p = .002) and E-selectin (p = .006) compared with the control group.	coq	34-39	selectin E	Homo sapiens	107-117
33285023-5	2021	The visual system seems to be mainly involved when the first steps of CoQ10 synthesis are impaired (PDSS1, PDSS2, and COQ2 deficiency).	coq	70-75	decaprenyl diphosphate synthase subunit 2	Homo sapiens	107-112
32306167-8	2021	Interestingly, although CoQ10 supplementation (5 muM) was able to restore cellular CoQ10 status and CS activity to control levels following OP treatment, complex II+III activity was only restored to control levels in neuronal cells exposed to dichlorvos (50 microM).	coq	24-29	citrate synthase	Homo sapiens	100-102
32306167-11	2021	Although CoQ10 supplementation was able to ameliorate OP induced deficiencies in CS activity, ETC complex II+III activity appeared partially refractory to this treatment.	coq	9-14	citrate synthase	Homo sapiens	81-83
33113448-7	2021	Mitochondrial function of oocytes treated by 50 muM CoQ10 could be boosted, through increasing the levels of mitochondrial membrane potential, ATP production and CoQ6, and changing the pattern of mitochondrial distribution as well.	coq	52-57	coenzyme Q6, monooxygenase	Sus scrofa	162-166
33271250-6	2021	The results showed that hepatic CoQ10 levels were decreased during the APAP-induced hepatotoxicity and preceded serum ALT elevation.	coq	32-37	glutamic pyruvic transaminase, soluble	Mus musculus	118-121
32697403-0	2020	Implication of Nrf2/HO-1 pathway in the protective effects of coenzyme Q10 against preeclampsia-like in a rat model.	coq	62-74	NFE2 like bZIP transcription factor 2	Rattus norvegicus	15-19
32975579-4	2020	This finding leads us to hypothesize that the therapeutic effects of CoQ10, frequently administered to patients with primary or secondary mitochondrial dysfunction, might be due to its function as cofactor for sulfide:quinone oxidoreductase (SQOR), the first enzyme in the sulfide oxidation pathway.	coq	69-74	crystallin zeta	Homo sapiens	218-240
32975579-4	2020	This finding leads us to hypothesize that the therapeutic effects of CoQ10, frequently administered to patients with primary or secondary mitochondrial dysfunction, might be due to its function as cofactor for sulfide:quinone oxidoreductase (SQOR), the first enzyme in the sulfide oxidation pathway.	coq	69-74	sulfide quinone oxidoreductase	Homo sapiens	242-246
32975579-5	2020	Here, using biased and unbiased approaches, we show that supraphysiological levels of CoQ10 induces an increase in the expression of SQOR in skin fibroblasts from control subjects and patients with mutations in Complex I subunits genes or CoQ biosynthetic genes.	coq	86-91	sulfide quinone oxidoreductase	Homo sapiens	133-137
32975579-7	2020	These metabolic changes are independent of the presence of sulfur aminoacids, are confirmed in mouse models, and are recapitulated by overexpression of SQOR, further proving that the metabolic effects of CoQ10 supplementation are mediated by the overexpression of SQOR.	coq	204-209	sulfide quinone oxidoreductase	Mus musculus	152-156
32975579-7	2020	These metabolic changes are independent of the presence of sulfur aminoacids, are confirmed in mouse models, and are recapitulated by overexpression of SQOR, further proving that the metabolic effects of CoQ10 supplementation are mediated by the overexpression of SQOR.	coq	204-209	sulfide quinone oxidoreductase	Mus musculus	264-268
33187177-7	2020	As the coenzyme Q10 treatment concentration increased, the number of cells per unit area and the thickness of the epidermal layer increased, the expression level of filaggrin increased, and the contraction rate of full-thickness HSE was proportional to the amount of TGF beta-1 secreted.	coq	7-19	filaggrin	Homo sapiens	165-174
33187177-7	2020	As the coenzyme Q10 treatment concentration increased, the number of cells per unit area and the thickness of the epidermal layer increased, the expression level of filaggrin increased, and the contraction rate of full-thickness HSE was proportional to the amount of TGF beta-1 secreted.	coq	7-19	transforming growth factor beta 1	Homo sapiens	267-277
33182307-0	2020	Human Microfibrillar-Associated Protein 4 (MFAP4) Gene Promoter: A TATA-Less Promoter That Is Regulated by Retinol and Coenzyme Q10 in Human Fibroblast Cells.	coq	119-131	microfibril associated protein 4	Homo sapiens	6-41
33182307-0	2020	Human Microfibrillar-Associated Protein 4 (MFAP4) Gene Promoter: A TATA-Less Promoter That Is Regulated by Retinol and Coenzyme Q10 in Human Fibroblast Cells.	coq	119-131	microfibril associated protein 4	Homo sapiens	43-48
33156836-9	2020	Th17 cell and phosphorylated STAT3-expressed cell populations were also decreased in LGNP-CoQ10 injected mice.	coq	90-95	signal transducer and activator of transcription 3	Mus musculus	29-34
33381582-9	2020	Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1beta, oligomerization domain-like receptor 3 and nucleotide-binding, interleukin-6, and tumor necrosis factor-alpha expression levels; coenzyme Q10 also increased beclin 1 levels.	coq	0-12	sequestosome 1	Mus musculus	54-68
33381582-9	2020	Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1beta, oligomerization domain-like receptor 3 and nucleotide-binding, interleukin-6, and tumor necrosis factor-alpha expression levels; coenzyme Q10 also increased beclin 1 levels.	coq	0-12	interleukin 1 beta	Mus musculus	70-87
33381582-9	2020	Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1beta, oligomerization domain-like receptor 3 and nucleotide-binding, interleukin-6, and tumor necrosis factor-alpha expression levels; coenzyme Q10 also increased beclin 1 levels.	coq	0-12	interleukin 6	Mus musculus	152-165
33381582-9	2020	Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1beta, oligomerization domain-like receptor 3 and nucleotide-binding, interleukin-6, and tumor necrosis factor-alpha expression levels; coenzyme Q10 also increased beclin 1 levels.	coq	0-12	tumor necrosis factor	Mus musculus	171-198
33381582-9	2020	Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1beta, oligomerization domain-like receptor 3 and nucleotide-binding, interleukin-6, and tumor necrosis factor-alpha expression levels; coenzyme Q10 also increased beclin 1 levels.	coq	0-12	beclin 1, autophagy related	Mus musculus	246-254
33328587-8	2021	We found that degradation of FA by formaldehyde scavenger-NaHSO3 or coenzyme Q10 reduced Abeta aggregation and ameliorated the neurotoxicity, and improved the cognitive performance in APP/PS1 mice.	coq	68-80	presenilin 1	Mus musculus	188-191
33317156-16	2020	In individuals with a deficiency of selenium and coenzyme Q10, low selenium status is related to impaired renal function, and thus supplementation with selenium and coenzyme Q10 results in significantly improved renal function as seen from creatinine and cystatin-C and through the CKD-EPI algorithm.	coq	165-177	cystatin C	Homo sapiens	255-265
33036883-9	2020	This result indicates that the intestinal absorption of CoQ10 is mediated by NPC1L1.	coq	56-61	NPC1 like intracellular cholesterol transporter 1	Rattus norvegicus	77-83
32829089-9	2020	Furthermore, Q10 reduced the infiltration of immune cells such as monocytes and neutrophils and augmentation of chemokines such as CC chemokine-2 (CCL2) and C-X-C chemokine-2 (CXCL2) in pancreas of AP mice.	coq	13-16	chemokine (C-C motif) ligand 2	Mus musculus	147-151
32829089-9	2020	Furthermore, Q10 reduced the infiltration of immune cells such as monocytes and neutrophils and augmentation of chemokines such as CC chemokine-2 (CCL2) and C-X-C chemokine-2 (CXCL2) in pancreas of AP mice.	coq	13-16	chemokine (C-X-C motif) ligand 2	Mus musculus	176-181
32697403-7	2020	RESULTS: Coenzyme Q10-treatment decreased the blood pressure in rat model with preeclampsia by regulating the circulating levels of sFlt-1 and PlGF.	coq	9-21	placental growth factor	Rattus norvegicus	143-147
32697403-9	2020	Coenzyme Q10 activated the placental Nrf2/HO-1 pathway in L-NAME-induced preeclampsia rats.	coq	0-12	NFE2 like bZIP transcription factor 2	Rattus norvegicus	37-41
32697403-9	2020	Coenzyme Q10 activated the placental Nrf2/HO-1 pathway in L-NAME-induced preeclampsia rats.	coq	0-12	heme oxygenase 1	Rattus norvegicus	42-46
32697403-10	2020	CONCLUSION: Coenzyme Q10 attenuated placental inflammatory and oxidative stress, thereby protecting the rats against preeclampsia by activating the Nrf2/HO-1 pathway.	coq	12-24	NFE2 like bZIP transcription factor 2	Rattus norvegicus	148-152
32697403-10	2020	CONCLUSION: Coenzyme Q10 attenuated placental inflammatory and oxidative stress, thereby protecting the rats against preeclampsia by activating the Nrf2/HO-1 pathway.	coq	12-24	heme oxygenase 1	Rattus norvegicus	153-157
32697403-0	2020	Implication of Nrf2/HO-1 pathway in the protective effects of coenzyme Q10 against preeclampsia-like in a rat model.	coq	62-74	heme oxygenase 1	Rattus norvegicus	20-24
32994821-0	2020	Hydrogen gas activates coenzyme Q10 to restore exhausted CD8+ T cells, especially PD-1+Tim3+terminal CD8+ T cells, leading to better nivolumab outcomes in patients with lung cancer.	coq	23-35	CD8a molecule	Homo sapiens	57-60
33080906-6	2020	Results: The administration of the association of silymarin, vitamin C, vitamin E, coenzyme Q10 and selenomethionine (Medronys epato ) was effective since it showed a significant reduction of the evaluated parameters of ALT, AST, ALP and GGT, a significant improvement of lipid parameters, evaluated as markers of liver function, and improvements of ultrasonographic results.	coq	83-95	solute carrier family 17 member 5	Homo sapiens	225-228
33080906-6	2020	Results: The administration of the association of silymarin, vitamin C, vitamin E, coenzyme Q10 and selenomethionine (Medronys epato ) was effective since it showed a significant reduction of the evaluated parameters of ALT, AST, ALP and GGT, a significant improvement of lipid parameters, evaluated as markers of liver function, and improvements of ultrasonographic results.	coq	83-95	alkaline phosphatase, placental	Homo sapiens	230-233
33080906-6	2020	Results: The administration of the association of silymarin, vitamin C, vitamin E, coenzyme Q10 and selenomethionine (Medronys epato ) was effective since it showed a significant reduction of the evaluated parameters of ALT, AST, ALP and GGT, a significant improvement of lipid parameters, evaluated as markers of liver function, and improvements of ultrasonographic results.	coq	83-95	gamma-glutamyltransferase 1	Homo sapiens	238-241
33052507-0	2022	Effect of Statin Therapy on the Plasma Concentrations of Retinol, Alpha-Tocopherol and Coenzyme Q10 in Children with Familial Hypercholesterolemia.	coq	87-99	low density lipoprotein receptor	Homo sapiens	117-146
33052507-5	2022	The aim of this study was to evaluate the influence of statin treatment in children with FH on plasma concentrations of antioxidant vitamins: retinol, alpha-tocopherol and coenzyme Q10.	coq	172-184	low density lipoprotein receptor	Homo sapiens	89-91
32804429-2	2020	It is caused by mutations in the ETFA, ETFB, or ETFDH genes which are involved in the transfer of electrons from 11 flavin-containing dehydrogenases to Coenzyme Q10 (CoQ10 ) of the mitochondrial electron transport chain (ETC).	coq	152-164	electron transfer flavoprotein subunit alpha	Homo sapiens	33-37
33050406-10	2020	The results imply that the uptake of exogenous CoQ10 into the brain might be improved by the administration of LDLR inhibitors, or by interventions to stimulate luminal activity of SR-B1 transporters.	coq	47-52	low density lipoprotein receptor	Homo sapiens	111-115
33050406-10	2020	The results imply that the uptake of exogenous CoQ10 into the brain might be improved by the administration of LDLR inhibitors, or by interventions to stimulate luminal activity of SR-B1 transporters.	coq	47-52	scavenger receptor class B member 1	Homo sapiens	181-186
32804429-2	2020	It is caused by mutations in the ETFA, ETFB, or ETFDH genes which are involved in the transfer of electrons from 11 flavin-containing dehydrogenases to Coenzyme Q10 (CoQ10 ) of the mitochondrial electron transport chain (ETC).	coq	152-164	electron transfer flavoprotein subunit beta	Homo sapiens	39-43
32804429-2	2020	It is caused by mutations in the ETFA, ETFB, or ETFDH genes which are involved in the transfer of electrons from 11 flavin-containing dehydrogenases to Coenzyme Q10 (CoQ10 ) of the mitochondrial electron transport chain (ETC).	coq	152-164	electron transfer flavoprotein dehydrogenase	Homo sapiens	48-53
32804429-2	2020	It is caused by mutations in the ETFA, ETFB, or ETFDH genes which are involved in the transfer of electrons from 11 flavin-containing dehydrogenases to Coenzyme Q10 (CoQ10 ) of the mitochondrial electron transport chain (ETC).	coq	166-171	electron transfer flavoprotein subunit alpha	Homo sapiens	33-37
32804429-2	2020	It is caused by mutations in the ETFA, ETFB, or ETFDH genes which are involved in the transfer of electrons from 11 flavin-containing dehydrogenases to Coenzyme Q10 (CoQ10 ) of the mitochondrial electron transport chain (ETC).	coq	166-171	electron transfer flavoprotein subunit beta	Homo sapiens	39-43
32804429-2	2020	It is caused by mutations in the ETFA, ETFB, or ETFDH genes which are involved in the transfer of electrons from 11 flavin-containing dehydrogenases to Coenzyme Q10 (CoQ10 ) of the mitochondrial electron transport chain (ETC).	coq	166-171	electron transfer flavoprotein dehydrogenase	Homo sapiens	48-53
32961568-0	2020	Evaluation of Efficacy of Coenzyme Q10 as an Adjunct to Nonsurgical Periodontal Therapy and Its Effect on Crevicular Superoxide Dismutase in Patients with Chronic Periodontitis.	coq	26-38	superoxide dismutase 1	Homo sapiens	117-137
32279354-9	2020	Furthermore, we found CIRBP mediated cardiac ubiquinone (CoQ10 ) biosynthesis play an important role in extending heart preservation and ubiquinone biosynthesis protein COQ9 was an essential down-stream regulator during this process.	coq	57-62	cold inducible RNA binding protein	Rattus norvegicus	22-27
32279354-9	2020	Furthermore, we found CIRBP mediated cardiac ubiquinone (CoQ10 ) biosynthesis play an important role in extending heart preservation and ubiquinone biosynthesis protein COQ9 was an essential down-stream regulator during this process.	coq	57-62	coenzyme Q9	Rattus norvegicus	169-173
32279354-10	2020	Finally, we found that zr17-2, a CIRBP agonist, could enhance the expression of CIRBP, which further enhances the synthesis of CoQ10 and promotes scavenge of reactive oxygen species and ATP production to extend the heart preservation.	coq	127-132	cold inducible RNA binding protein	Rattus norvegicus	33-38
32279354-10	2020	Finally, we found that zr17-2, a CIRBP agonist, could enhance the expression of CIRBP, which further enhances the synthesis of CoQ10 and promotes scavenge of reactive oxygen species and ATP production to extend the heart preservation.	coq	127-132	cold inducible RNA binding protein	Rattus norvegicus	80-85
32553579-2	2020	A biallelic pathogenic variant of COQ8A gene causes the occurrence of the primary coenzyme Q10 deficiency type 4.	coq	82-94	coenzyme Q8A	Homo sapiens	34-39
32553579-9	2020	CONCLUSION: The p.Gln279Pro was detected in the KxGQ motif and the QKE triplet of the COQ8A protein, whose structures were crucial for the structure and function of the COQ8A protein associated with the biosynthesis of coenzyme Q10 and the proband"s clinical symptoms were relatively milder than those previously reported.	coq	219-231	coenzyme Q8A	Homo sapiens	86-91
32553579-9	2020	CONCLUSION: The p.Gln279Pro was detected in the KxGQ motif and the QKE triplet of the COQ8A protein, whose structures were crucial for the structure and function of the COQ8A protein associated with the biosynthesis of coenzyme Q10 and the proband"s clinical symptoms were relatively milder than those previously reported.	coq	219-231	coenzyme Q8A	Homo sapiens	169-174
32399598-9	2020	The remaining patients had variants in candidate genes such as TFAM, involved in mtDNA transcription, replication, and packaging, and GGPS1 involved in mevalonate/coenzyme Q10 biosynthesis and whose enzymatic product is required for mouse folliculogenesis.	coq	163-175	geranylgeranyl diphosphate synthase 1	Homo sapiens	134-139
32961568-1	2020	OBJECTIVES:  To assess the efficacy of coenzyme Q10 (CoQ10) as an adjunct to nonsurgical periodontal therapy and its effect on superoxide dismutase (SOD) in gingival crevicular fluid (GCF) in patients with chronic periodontitis (CP).	coq	39-51	superoxide dismutase 1	Homo sapiens	127-147
32961568-1	2020	OBJECTIVES:  To assess the efficacy of coenzyme Q10 (CoQ10) as an adjunct to nonsurgical periodontal therapy and its effect on superoxide dismutase (SOD) in gingival crevicular fluid (GCF) in patients with chronic periodontitis (CP).	coq	39-51	superoxide dismutase 1	Homo sapiens	149-152
32961568-1	2020	OBJECTIVES:  To assess the efficacy of coenzyme Q10 (CoQ10) as an adjunct to nonsurgical periodontal therapy and its effect on superoxide dismutase (SOD) in gingival crevicular fluid (GCF) in patients with chronic periodontitis (CP).	coq	53-58	superoxide dismutase 1	Homo sapiens	127-147
32961568-1	2020	OBJECTIVES:  To assess the efficacy of coenzyme Q10 (CoQ10) as an adjunct to nonsurgical periodontal therapy and its effect on superoxide dismutase (SOD) in gingival crevicular fluid (GCF) in patients with chronic periodontitis (CP).	coq	53-58	superoxide dismutase 1	Homo sapiens	149-152
32920026-0	2021	NT-Pro BNP Predicts Myocardial Injury Post-vascular Surgery and is Reduced with CoQ 10.	coq	80-86	natriuretic peptide B	Homo sapiens	7-10
32718232-0	2020	Co Q10 improves vascular reactivity in male diabetic rats by enhancing insulin sensitivity and antioxidant effect.	coq	0-6	insulin	Homo sapiens	71-78
32337771-9	2020	CoQ10 treatment led to improvement by clinical report in 14 of 30 patients, and by quantitative longitudinal assessments in 8 of 11 patients (SARA: -0.81/year).	coq	0-5	secretion associated Ras related GTPase 1A	Homo sapiens	142-146
32923487-8	2020	In contrast, CoQ10 sunscreen prevented from UVB-induced skin damage, as well as reversing SOD, GSH-Px, and MDA activities, and MMP-1 and DNMT1 levels.	coq	13-18	matrix metallopeptidase 13	Mus musculus	127-132
32923487-8	2020	In contrast, CoQ10 sunscreen prevented from UVB-induced skin damage, as well as reversing SOD, GSH-Px, and MDA activities, and MMP-1 and DNMT1 levels.	coq	13-18	DNA methyltransferase (cytosine-5) 1	Mus musculus	137-142
32718232-3	2020	This study was designed to evaluate the effect of Co-Q10 administration to improve vascular complications and increase insulin sensitivity in diabetic rats.	coq	50-56	insulin	Homo sapiens	119-126
32718232-8	2020	Combined Co-Q10 with insulin was found to increase insulin sensitivity and decrease its resistance, which helps to decrease insulin doses in diabetic patients and reduce its side effects.	coq	9-15	insulin	Homo sapiens	51-58
32718232-8	2020	Combined Co-Q10 with insulin was found to increase insulin sensitivity and decrease its resistance, which helps to decrease insulin doses in diabetic patients and reduce its side effects.	coq	9-15	insulin	Homo sapiens	51-58
32792941-0	2020	CoenzymeQ10-Induced Activation of AMPK-YAP-OPA1 Pathway Alleviates Atherosclerosis by Improving Mitochondrial Function, Inhibiting Oxidative Stress and Promoting Energy Metabolism.	coq	0-11	yes-associated protein 1	Mus musculus	39-42
32792941-0	2020	CoenzymeQ10-Induced Activation of AMPK-YAP-OPA1 Pathway Alleviates Atherosclerosis by Improving Mitochondrial Function, Inhibiting Oxidative Stress and Promoting Energy Metabolism.	coq	0-11	OPA1, mitochondrial dynamin like GTPase	Mus musculus	43-47
32792941-5	2020	Both in high fat diet (HFD) fed APOE -/- mice and in ox-LDL-treated HAECs, CoQ10 significantly decreased the levels of TG, TC and LDL-C and increased the levels of HDL-C, thus playing a role in regulating lipid homeostasis.	coq	75-80	apolipoprotein E	Mus musculus	32-36
32792941-8	2020	CoQ10 also decreased the levels of related inflammatory factors (ICAM-1, VCAM-1, IL-6, TNF-alpha and NLRP3).	coq	0-5	intercellular adhesion molecule 1	Mus musculus	65-71
32792941-8	2020	CoQ10 also decreased the levels of related inflammatory factors (ICAM-1, VCAM-1, IL-6, TNF-alpha and NLRP3).	coq	0-5	vascular cell adhesion molecule 1	Mus musculus	73-79
32792941-8	2020	CoQ10 also decreased the levels of related inflammatory factors (ICAM-1, VCAM-1, IL-6, TNF-alpha and NLRP3).	coq	0-5	interleukin 6	Mus musculus	81-85
32792941-8	2020	CoQ10 also decreased the levels of related inflammatory factors (ICAM-1, VCAM-1, IL-6, TNF-alpha and NLRP3).	coq	0-5	tumor necrosis factor	Mus musculus	87-96
32792941-8	2020	CoQ10 also decreased the levels of related inflammatory factors (ICAM-1, VCAM-1, IL-6, TNF-alpha and NLRP3).	coq	0-5	NLR family, pyrin domain containing 3	Mus musculus	101-106
32792941-10	2020	The further study suggested AMPK small interfering RNA (siRNA) and YAP small interfering RNA (siRNA) affected the expression of OPA1, a crucial protein regulating the balance of mitochondrial fusion and division and decreased the therapeutic effects of CoQ10.	coq	253-258	yes-associated protein 1	Mus musculus	67-70
32792941-10	2020	The further study suggested AMPK small interfering RNA (siRNA) and YAP small interfering RNA (siRNA) affected the expression of OPA1, a crucial protein regulating the balance of mitochondrial fusion and division and decreased the therapeutic effects of CoQ10.	coq	253-258	OPA1, mitochondrial dynamin like GTPase	Mus musculus	128-132
32792941-11	2020	These results indicated that CoQ10 improved mitochondrial function, inhibited ROS production, promoted energy metabolism and attenuated AS by activating AMPK-YAP-OPA1 pathway.	coq	29-34	yes-associated protein 1	Mus musculus	158-161
32792941-11	2020	These results indicated that CoQ10 improved mitochondrial function, inhibited ROS production, promoted energy metabolism and attenuated AS by activating AMPK-YAP-OPA1 pathway.	coq	29-34	OPA1, mitochondrial dynamin like GTPase	Mus musculus	162-166
32377738-14	2020	CoQ10 improved energy replenishment and inhibited oxidative stress, which may lead to a decrease in ApoE and phosphorylated tau protein expression, thus mitigating the sevoflurane-induced neuroinflammation in mouse hippocampal neurons.	coq	0-5	apolipoprotein E	Mus musculus	100-104
32764923-5	2020	Methods: We tested cardioprotective and hepatoprotective effects of CoQ10-loaded nano-carriers against Doxorubicin and Trastuzumab toxicities in cardiomyocytes and liver cells through analysis of cell viability, lipid peroxidation, expression of leukotrienes, p65/NF-kB and pro-inflammatory cytokines involved in anticancer-induced cardio and hepatotoxicity.	coq	68-73	RELA proto-oncogene, NF-kB subunit	Homo sapiens	260-263
32764923-8	2020	CoQ10-loaded nano-emulsions showed also strong anti-inflammatory effects reducing leukotriene B4 and p65/NF-kappaB expression and Interleukin 1beta and 6 production during anticancer treatments.	coq	0-5	RELA proto-oncogene, NF-kB subunit	Homo sapiens	101-104
32764923-8	2020	CoQ10-loaded nano-emulsions showed also strong anti-inflammatory effects reducing leukotriene B4 and p65/NF-kappaB expression and Interleukin 1beta and 6 production during anticancer treatments.	coq	0-5	nuclear factor kappa B subunit 1	Homo sapiens	105-114
32764923-8	2020	CoQ10-loaded nano-emulsions showed also strong anti-inflammatory effects reducing leukotriene B4 and p65/NF-kappaB expression and Interleukin 1beta and 6 production during anticancer treatments.	coq	0-5	interleukin 1 beta	Homo sapiens	130-153
32473608-0	2020	Protective effects of Coenzyme Q10 against sevoflurane-induced cognitive impairment through regulating apolipoprotein E and phosphorylated Tau expression in young mice.	coq	22-34	apolipoprotein E	Mus musculus	103-119
30852912-10	2020	Topical CoQ10 + Vit.E treatment also decreased Iba1 expression in the retina of mechanic optic nerve injury groups.	coq	8-13	allograft inflammatory factor 1	Rattus norvegicus	47-51
31973572-7	2020	Adiponectin and PPARalpha gene expression exhibited a linear increased by increased levels of CoQ10.In conclusion, addition of CoQ10 to the diet influenced lipid metabolism and expression of the adiponectin and PPAR-alpha genes, which might be partially due to the improvement in mitochondrial metabolism and energy production.	coq	94-99	adiponectin, C1Q and collagen domain containing	Gallus gallus	0-11
31973572-7	2020	Adiponectin and PPARalpha gene expression exhibited a linear increased by increased levels of CoQ10.In conclusion, addition of CoQ10 to the diet influenced lipid metabolism and expression of the adiponectin and PPAR-alpha genes, which might be partially due to the improvement in mitochondrial metabolism and energy production.	coq	94-99	peroxisome proliferator activated receptor alpha	Gallus gallus	16-25
31973572-7	2020	Adiponectin and PPARalpha gene expression exhibited a linear increased by increased levels of CoQ10.In conclusion, addition of CoQ10 to the diet influenced lipid metabolism and expression of the adiponectin and PPAR-alpha genes, which might be partially due to the improvement in mitochondrial metabolism and energy production.	coq	94-99	adiponectin, C1Q and collagen domain containing	Gallus gallus	195-206
31973572-7	2020	Adiponectin and PPARalpha gene expression exhibited a linear increased by increased levels of CoQ10.In conclusion, addition of CoQ10 to the diet influenced lipid metabolism and expression of the adiponectin and PPAR-alpha genes, which might be partially due to the improvement in mitochondrial metabolism and energy production.	coq	94-99	peroxisome proliferator activated receptor alpha	Gallus gallus	211-221
31973572-7	2020	Adiponectin and PPARalpha gene expression exhibited a linear increased by increased levels of CoQ10.In conclusion, addition of CoQ10 to the diet influenced lipid metabolism and expression of the adiponectin and PPAR-alpha genes, which might be partially due to the improvement in mitochondrial metabolism and energy production.	coq	127-132	adiponectin, C1Q and collagen domain containing	Gallus gallus	0-11
31973572-7	2020	Adiponectin and PPARalpha gene expression exhibited a linear increased by increased levels of CoQ10.In conclusion, addition of CoQ10 to the diet influenced lipid metabolism and expression of the adiponectin and PPAR-alpha genes, which might be partially due to the improvement in mitochondrial metabolism and energy production.	coq	127-132	peroxisome proliferator activated receptor alpha	Gallus gallus	16-25
31973572-7	2020	Adiponectin and PPARalpha gene expression exhibited a linear increased by increased levels of CoQ10.In conclusion, addition of CoQ10 to the diet influenced lipid metabolism and expression of the adiponectin and PPAR-alpha genes, which might be partially due to the improvement in mitochondrial metabolism and energy production.	coq	127-132	adiponectin, C1Q and collagen domain containing	Gallus gallus	195-206
31973572-7	2020	Adiponectin and PPARalpha gene expression exhibited a linear increased by increased levels of CoQ10.In conclusion, addition of CoQ10 to the diet influenced lipid metabolism and expression of the adiponectin and PPAR-alpha genes, which might be partially due to the improvement in mitochondrial metabolism and energy production.	coq	127-132	peroxisome proliferator activated receptor alpha	Gallus gallus	211-221
31989689-1	2020	The current study aimed to test the profile of serum lipids, phospholipase D (PLD) activity, and CD59 expression pattern in rat hepatocellular carcinoma (HCC) after therapeutic treatment with Coenzyme Q10 (CoQ10).	coq	192-204	CD59 molecule	Rattus norvegicus	97-101
31989689-1	2020	The current study aimed to test the profile of serum lipids, phospholipase D (PLD) activity, and CD59 expression pattern in rat hepatocellular carcinoma (HCC) after therapeutic treatment with Coenzyme Q10 (CoQ10).	coq	206-211	CD59 molecule	Rattus norvegicus	97-101
31989689-6	2020	CoQ10 reduced the cell proliferation, histological alterations, and the levels of AFP and TNF-alpha but increased lipids, CH50, and sCD59 in serum.	coq	0-5	alpha-fetoprotein	Rattus norvegicus	82-85
31989689-6	2020	CoQ10 reduced the cell proliferation, histological alterations, and the levels of AFP and TNF-alpha but increased lipids, CH50, and sCD59 in serum.	coq	0-5	tumor necrosis factor	Rattus norvegicus	90-99
31989689-7	2020	In the liver cell, CoQ10 decreased and increased PLD and HMGCR enzyme activities, respectively.	coq	19-24	3-hydroxy-3-methylglutaryl-CoA reductase	Rattus norvegicus	57-62
31989689-9	2020	Statistical correlation indicated an inverse relationship between CH50 and each of CD59 expression and PLD activity after treatment with CoQ10.	coq	137-142	CD59 molecule	Rattus norvegicus	83-87
31989689-10	2020	In conclusion, CoQ10 could protect against rat HCC through increased lipids and the reduction of CD59 expression and PLD activity.	coq	15-20	CD59 molecule	Rattus norvegicus	97-101
31989689-11	2020	SIGNIFICANCE OF THE STUDY: To our knowledge, this study is the first to describe the attenuating effect of antitumour natural product like Coenzyme Q10 (CoQ10) via the reduction of CD59 expression and phospholipase D (PLD) activity.	coq	153-158	CD59 molecule	Rattus norvegicus	181-185
32381600-1	2020	BACKGROUND: Mutations in ADCK4 (aarF domain containing kinase 4) generally manifest as steroid-resistant nephrotic syndrome and induce coenzyme Q10 (CoQ10) deficiency.	coq	135-147	coenzyme Q8B	Mus musculus	25-30
32381600-1	2020	BACKGROUND: Mutations in ADCK4 (aarF domain containing kinase 4) generally manifest as steroid-resistant nephrotic syndrome and induce coenzyme Q10 (CoQ10) deficiency.	coq	135-147	coenzyme Q8B	Mus musculus	32-63
32381600-1	2020	BACKGROUND: Mutations in ADCK4 (aarF domain containing kinase 4) generally manifest as steroid-resistant nephrotic syndrome and induce coenzyme Q10 (CoQ10) deficiency.	coq	149-154	coenzyme Q8B	Mus musculus	25-30
32381600-1	2020	BACKGROUND: Mutations in ADCK4 (aarF domain containing kinase 4) generally manifest as steroid-resistant nephrotic syndrome and induce coenzyme Q10 (CoQ10) deficiency.	coq	149-154	coenzyme Q8B	Mus musculus	32-63
32381600-7	2020	In vitro studies revealed that ADCK4-knockout podocytes had significantly reduced CoQ10 concentration, respiratory chain activity, and mitochondrial potential, and subsequently displayed an increase in the number of dysmorphic mitochondria.	coq	82-87	coenzyme Q8B	Mus musculus	31-36
32381600-11	2020	CONCLUSIONS: Our study shows that ADCK4 is required for CoQ10 biosynthesis and mitochondrial function in podocytes, and suggests that ADCK4 in podocytes stabilizes proteins in complex Q in podocytes.	coq	56-61	coenzyme Q8B	Mus musculus	34-39
32377738-0	2020	Coenzyme Q10 alleviates sevoflurane-induced neuroinflammation by regulating the levels of apolipoprotein E and phosphorylated tau protein in mouse hippocampal neurons.	coq	0-12	apolipoprotein E	Mus musculus	90-106
32383521-0	2020	Biotin, coenzyme Q10, and their combination ameliorate aluminium chloride-induced Alzheimer"s disease via attenuating neuroinflammation and improving brain insulin signaling.	coq	8-20	insulin	Homo sapiens	156-163
32383521-13	2020	In conclusion, biotin and CoQ10 could protect against AD via attenuating inflammatory response and enhancing insulin signaling.	coq	26-31	insulin	Homo sapiens	109-116
32375340-4	2020	Results from the current meta-analysis, involving 318 participants, showed that CoQ10 supplementation in individuals with metabolic syndrome increased adiponectin levels when compared to those on placebo (SMD: 1.44 [95% CI: -0.13, 3.00]; I2 = 96%, p < 0.00001).	coq	80-85	adiponectin, C1Q and collagen domain containing	Homo sapiens	151-162
32342825-7	2021	Therefore, current review specially targeted in the investigation of clinical and pre-clinical features available for ALS to understand the pathogenic mechanisms and to explore the pharmacological interventions associated with up-regulation of intracellular adenyl cyclase/cAMP/CREB and mitochondrial-ETC coenzyme-Q10 activation as a future drug target in the amelioration of ALS mediated motor neuronal dysfunctions.	coq	305-317	cathelicidin antimicrobial peptide	Homo sapiens	273-277
32342825-7	2021	Therefore, current review specially targeted in the investigation of clinical and pre-clinical features available for ALS to understand the pathogenic mechanisms and to explore the pharmacological interventions associated with up-regulation of intracellular adenyl cyclase/cAMP/CREB and mitochondrial-ETC coenzyme-Q10 activation as a future drug target in the amelioration of ALS mediated motor neuronal dysfunctions.	coq	305-317	cAMP responsive element binding protein 1	Homo sapiens	278-282
32331285-4	2020	Therefore, exogenous CoQ10 supplementation might be useful as an adjuvant in the treatment of cardiovascular diseases such as heart failure, atrial fibrillation, and myocardial infarction and in associated risk factors such as hypertension, insulin resistance, dyslipidemias, and obesity.	coq	21-26	insulin	Homo sapiens	241-248
32473608-12	2020	The results indicated that the injection of CoQ10 ahead of sevoflurane treatment could reversed the anesthesia induced energy deficiency, mitochondrial dysfunction, ApoE and its fragments expression, Abeta1-42 generation, Tau phosphorylation and cognitive impairment in young mice.	coq	44-49	apolipoprotein E	Mus musculus	165-169
32473608-14	2020	CoQ10 could reduce ApoE expression by improving energy replenishment and mitochondrial functions, thereby alleviating sevoflurane-induced brain damage and cognitive impairment.	coq	0-5	apolipoprotein E	Mus musculus	19-23
32074388-3	2020	These particles, termed CoQ10 nanodisks (ND), contain 1.0 mg CoQ10 /5 mg PtdCho/2 mg apoA-I (97% CoQ10 solubilization efficiency).	coq	24-29	apolipoprotein A1	Homo sapiens	85-91
31852725-3	2020	CoQ10 significantly reduces BPA-induced elevated levels of germ cell apoptosis, phosphorylated checkpoint kinase 1 (CHK-1), double-strand breaks (DSBs), and chromosome defects in diakinesis oocytes.	coq	0-5	Serine/threonine-protein kinase chk-1	Caenorhabditis elegans	95-114
31852725-3	2020	CoQ10 significantly reduces BPA-induced elevated levels of germ cell apoptosis, phosphorylated checkpoint kinase 1 (CHK-1), double-strand breaks (DSBs), and chromosome defects in diakinesis oocytes.	coq	0-5	Serine/threonine-protein kinase chk-1	Caenorhabditis elegans	116-121
31137081-0	2020	Successful maintenance of partial remission in a child with COQ2 nephropathy by coenzyme Q10 treatment.	coq	80-92	coenzyme Q2, polyprenyltransferase	Homo sapiens	60-64
32328242-3	2020	The aim was to evaluate CoQ10 supplementation effect on total antioxidant capacity (TAC), malondialdehyde (MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) levels using data collected from randomized controlled trials (RCTs).	coq	24-29	catalase	Homo sapiens	175-183
32328242-3	2020	The aim was to evaluate CoQ10 supplementation effect on total antioxidant capacity (TAC), malondialdehyde (MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) levels using data collected from randomized controlled trials (RCTs).	coq	24-29	catalase	Homo sapiens	185-188
32074388-5	2020	Incorporation of CoQ10 into ND resulted in quenching of apoA-I tryptophan fluorescence emission.	coq	17-22	apolipoprotein A1	Homo sapiens	56-62
31998536-7	2020	When miso soup containing P30 was provided, the serum CoQ10 concentration increased faster than when participants consumed other P30-containing soups or a P30-containing raw egg sauce.	coq	54-59	centromere protein V	Homo sapiens	26-29
31711704-13	2020	Dietary supplementation of CoQ10 linearly decreased seminal plasma ALAT and ASAT and linearly increased seminal plasma TAC.	coq	27-32	glutamic--pyruvic transaminase	Homo sapiens	67-71
31755492-0	2020	Coenzyme Q10 attenuates platelet integrin alphaIIbbeta3 signaling and platelet hyper-reactivity in ApoE-deficient mice.	coq	0-12	apolipoprotein E	Mus musculus	99-103
31755492-4	2020	We found that CoQ10 supplementation in ApoE-/- mice significantly alleviated formation of HFD-induced atherosclerotic lesions, and attenuated platelet hyper-aggregation and granule secretion, including CD62P, CD63 and CD40 ligand (CD40L) expression and platelet factor-4, beta-thromboglobulin and activation normal T cell expressed and secreted (CCL5) release.	coq	14-19	apolipoprotein E	Mus musculus	39-43
31755492-4	2020	We found that CoQ10 supplementation in ApoE-/- mice significantly alleviated formation of HFD-induced atherosclerotic lesions, and attenuated platelet hyper-aggregation and granule secretion, including CD62P, CD63 and CD40 ligand (CD40L) expression and platelet factor-4, beta-thromboglobulin and activation normal T cell expressed and secreted (CCL5) release.	coq	14-19	selectin, platelet	Mus musculus	202-207
31755492-4	2020	We found that CoQ10 supplementation in ApoE-/- mice significantly alleviated formation of HFD-induced atherosclerotic lesions, and attenuated platelet hyper-aggregation and granule secretion, including CD62P, CD63 and CD40 ligand (CD40L) expression and platelet factor-4, beta-thromboglobulin and activation normal T cell expressed and secreted (CCL5) release.	coq	14-19	CD40 ligand	Mus musculus	218-229
31755492-4	2020	We found that CoQ10 supplementation in ApoE-/- mice significantly alleviated formation of HFD-induced atherosclerotic lesions, and attenuated platelet hyper-aggregation and granule secretion, including CD62P, CD63 and CD40 ligand (CD40L) expression and platelet factor-4, beta-thromboglobulin and activation normal T cell expressed and secreted (CCL5) release.	coq	14-19	CD40 ligand	Mus musculus	231-236
31755492-4	2020	We found that CoQ10 supplementation in ApoE-/- mice significantly alleviated formation of HFD-induced atherosclerotic lesions, and attenuated platelet hyper-aggregation and granule secretion, including CD62P, CD63 and CD40 ligand (CD40L) expression and platelet factor-4, beta-thromboglobulin and activation normal T cell expressed and secreted (CCL5) release.	coq	14-19	chemokine (C-C motif) ligand 5	Mus musculus	346-350
31998536-8	2020	The area under the curve for serum CoQ10 during the first 5 h after consumption of the P30-containing miso soup was approximately 1.5 times larger than those after the consumption of other P30-containing meals.	coq	35-40	centromere protein V	Homo sapiens	87-90
31860468-1	2019	Background Coenzyme Q10 is a fat-soluble antioxidant that can help to prevent collagen and elastin damage and avoid wrinkles.	coq	11-23	elastin	Mus musculus	91-98
31890231-1	2019	Background: The recessive ataxia ARCA2 is a rare disorder characterized by Coenzyme Q10 (CoQ10) deficiency due to biallelic mutations in ADCK3 gene.	coq	75-87	coenzyme Q8A	Homo sapiens	137-142
31890231-1	2019	Background: The recessive ataxia ARCA2 is a rare disorder characterized by Coenzyme Q10 (CoQ10) deficiency due to biallelic mutations in ADCK3 gene.	coq	89-94	coenzyme Q8A	Homo sapiens	137-142
31890231-3	2019	Here we described the long-term motor outcome of 4 untreated ARCA2 patients prospectively followed-up for one year after starting CoQ10 oral supplementation (15 mg/kg/day).	coq	130-135	coenzyme Q8A	Homo sapiens	61-66
31890231-7	2019	Conclusions: Although preliminarily, this observation suggests that only prolonged and continuous CoQ10 supplementation may induce mild clinical effects on general motor features of ARCA2.	coq	98-103	coenzyme Q8A	Homo sapiens	182-187
31915512-7	2019	Our results demonstrate that CoQ10 treatment significantly decreases the expression of the proapoptotic proteins Bax and Caspase-3, as shown through TUNEL-positive staining and the products of oxidative stress (ROS), while increasing the expression of the antiapoptotic protein Bcl-2 and the products of antioxidation, such as glutathione (GSH), against apoptosis and oxidative stress, in a H2O2-induced model.	coq	29-34	BCL2 associated X, apoptosis regulator	Homo sapiens	113-116
31915512-7	2019	Our results demonstrate that CoQ10 treatment significantly decreases the expression of the proapoptotic proteins Bax and Caspase-3, as shown through TUNEL-positive staining and the products of oxidative stress (ROS), while increasing the expression of the antiapoptotic protein Bcl-2 and the products of antioxidation, such as glutathione (GSH), against apoptosis and oxidative stress, in a H2O2-induced model.	coq	29-34	caspase 3	Homo sapiens	121-130
31915512-7	2019	Our results demonstrate that CoQ10 treatment significantly decreases the expression of the proapoptotic proteins Bax and Caspase-3, as shown through TUNEL-positive staining and the products of oxidative stress (ROS), while increasing the expression of the antiapoptotic protein Bcl-2 and the products of antioxidation, such as glutathione (GSH), against apoptosis and oxidative stress, in a H2O2-induced model.	coq	29-34	BCL2 apoptosis regulator	Homo sapiens	278-283
32038732-0	2019	Possible antioxidant mechanism of coenzyme Q10 in diabetes: impact on Sirt1/Nrf2 signaling pathways.	coq	34-46	sirtuin 1	Rattus norvegicus	70-75
32038732-0	2019	Possible antioxidant mechanism of coenzyme Q10 in diabetes: impact on Sirt1/Nrf2 signaling pathways.	coq	34-46	NFE2 like bZIP transcription factor 2	Rattus norvegicus	76-80
32038732-2	2019	The aim of this study was to investigate potential antioxidant activity of coenzyme Q10 (Co Q10) against hyperglycemia-induced oxidative stress in diabetic rat and unraveling its mechanism of action by focusing on silent information regulator 1 (Sirt1) and nuclear factor E2-related factor 2 (Nrf2) mRNA expression level.	coq	75-87	sirtuin 1	Rattus norvegicus	246-251
32038732-2	2019	The aim of this study was to investigate potential antioxidant activity of coenzyme Q10 (Co Q10) against hyperglycemia-induced oxidative stress in diabetic rat and unraveling its mechanism of action by focusing on silent information regulator 1 (Sirt1) and nuclear factor E2-related factor 2 (Nrf2) mRNA expression level.	coq	75-87	NFE2 like bZIP transcription factor 2	Rattus norvegicus	293-297
32038732-2	2019	The aim of this study was to investigate potential antioxidant activity of coenzyme Q10 (Co Q10) against hyperglycemia-induced oxidative stress in diabetic rat and unraveling its mechanism of action by focusing on silent information regulator 1 (Sirt1) and nuclear factor E2-related factor 2 (Nrf2) mRNA expression level.	coq	89-95	sirtuin 1	Rattus norvegicus	246-251
32038732-2	2019	The aim of this study was to investigate potential antioxidant activity of coenzyme Q10 (Co Q10) against hyperglycemia-induced oxidative stress in diabetic rat and unraveling its mechanism of action by focusing on silent information regulator 1 (Sirt1) and nuclear factor E2-related factor 2 (Nrf2) mRNA expression level.	coq	89-95	NFE2 like bZIP transcription factor 2	Rattus norvegicus	293-297
32038732-8	2019	Co Q10 treatment significantly up-regulated Sirt1 and Nrf2 mRNA levels along with an increase in catalase activity in diabetic group as compared with untreated diabetic rats.	coq	0-6	sirtuin 1	Rattus norvegicus	44-49
32038732-8	2019	Co Q10 treatment significantly up-regulated Sirt1 and Nrf2 mRNA levels along with an increase in catalase activity in diabetic group as compared with untreated diabetic rats.	coq	0-6	NFE2 like bZIP transcription factor 2	Rattus norvegicus	54-58
32038732-10	2019	Our data demonstrated that Co Q10 may exert its antioxidant activity in diabetes through the induction of Sirt1/Nrf2 gene expression.	coq	27-33	sirtuin 1	Rattus norvegicus	106-111
32038732-10	2019	Our data demonstrated that Co Q10 may exert its antioxidant activity in diabetes through the induction of Sirt1/Nrf2 gene expression.	coq	27-33	NFE2 like bZIP transcription factor 2	Rattus norvegicus	112-116
31766751-1	2019	The aim of this study was to use Jumpstart Nutrition  bone supplementing combination with vitamin-K2 and coenzyme-Q10 characterized by an innovative delivery system that improves bioavailability of calcium-to-phosphorus ratio (CPR) and parathyroid hormone (PTH) in the management of osteoarthritis (OA).	coq	105-117	parathyroid hormone	Homo sapiens	236-255
31824163-0	2019	The Effect of Coenzyme Q10 Supplementation on Vascular Endothelial Growth Factor and Serum Levels of Interleukin 6 and 8 in Women with Breast Cancer: A Double-Blind, Placebo-Controlled, Randomized Clinical Trial.	coq	14-26	vascular endothelial growth factor A	Homo sapiens	46-80
31824163-0	2019	The Effect of Coenzyme Q10 Supplementation on Vascular Endothelial Growth Factor and Serum Levels of Interleukin 6 and 8 in Women with Breast Cancer: A Double-Blind, Placebo-Controlled, Randomized Clinical Trial.	coq	14-26	interleukin 6	Homo sapiens	101-120
31824163-9	2019	Supplementation with CoQ10 demonstrated a significant decrease in IL-8 and IL-6 serum levels compared to placebo (P&lt; 0.05).	coq	21-26	C-X-C motif chemokine ligand 8	Homo sapiens	66-70
31824163-9	2019	Supplementation with CoQ10 demonstrated a significant decrease in IL-8 and IL-6 serum levels compared to placebo (P&lt; 0.05).	coq	21-26	interleukin 6	Homo sapiens	75-79
31392559-9	2019	CONCLUSIONS: It seems that CoQ10 may provide a new complementary approach for RA patients.Key Points  CoQ10 supplementation in RA patients attenuated serum MMP-3 level.	coq	102-107	matrix metallopeptidase 3	Homo sapiens	156-161
31766751-1	2019	The aim of this study was to use Jumpstart Nutrition  bone supplementing combination with vitamin-K2 and coenzyme-Q10 characterized by an innovative delivery system that improves bioavailability of calcium-to-phosphorus ratio (CPR) and parathyroid hormone (PTH) in the management of osteoarthritis (OA).	coq	105-117	parathyroid hormone	Homo sapiens	257-260
31674935-6	2019	The combined use of TMZ and CoQ10 treatment was more effective than using either agent alone (p<0.01 for ROS, MDA, CAT, and cytosolic cyto-c; p<0.05 for SOD, nuclear Nrf2, and DeltaPsim loss).	coq	28-33	catalase	Rattus norvegicus	115-118
31674935-6	2019	The combined use of TMZ and CoQ10 treatment was more effective than using either agent alone (p<0.01 for ROS, MDA, CAT, and cytosolic cyto-c; p<0.05 for SOD, nuclear Nrf2, and DeltaPsim loss).	coq	28-33	NFE2 like bZIP transcription factor 2	Rattus norvegicus	166-170
31401771-9	2019	Treatment with 20 muM Q10 also decreased the activation of the PI3K/Akt/mTOR pathway.	coq	22-25	mechanistic target of rapamycin	Gallus gallus	72-76
31557371-0	2019	Upregulation of FSHR and PCNA by administration of coenzyme Q10 on cyclophosphamide-induced premature ovarian failure in a mouse model.	coq	51-63	follicle stimulating hormone receptor	Mus musculus	16-20
31557371-4	2019	However, little is known about the possible synergistic effect of CTX and CoQ10 on the expression of genes involved in folliculogenesis, such as proliferation cell nuclear antigen (PCNA) and follicle-stimulating hormone receptor (FSHR).	coq	74-79	proliferating cell nuclear antigen	Mus musculus	181-185
31557371-4	2019	However, little is known about the possible synergistic effect of CTX and CoQ10 on the expression of genes involved in folliculogenesis, such as proliferation cell nuclear antigen (PCNA) and follicle-stimulating hormone receptor (FSHR).	coq	74-79	follicle stimulating hormone receptor	Mus musculus	191-228
31634899-10	2019	In conclusion, FSP1/CoQ10/NAD(P)H exists as a stand-alone parallel system, which co-operates with GPX4 and glutathione (GSH) to suppress phospholipid peroxidation (pLPO) and ferroptosis.	coq	20-25	glutathione peroxidase 4	Homo sapiens	98-102
31695332-11	2019	In the group treated with the dietary supplement, CoQ10 plasma concentrations were inversely correlated with CPK levels, Clinical Index Score absolute values, and VAS.	coq	50-55	phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 alpha	Homo sapiens	109-112
31621627-1	2019	Cerebellar ataxia is a hallmark of coenzyme Q10 (CoQ10) deficiency associated with COQ8A mutations.	coq	35-47	coenzyme Q8A	Homo sapiens	83-88
31621627-1	2019	Cerebellar ataxia is a hallmark of coenzyme Q10 (CoQ10) deficiency associated with COQ8A mutations.	coq	49-54	coenzyme Q8A	Homo sapiens	83-88
31323021-2	2019	UbiA prenyltransferase domain-containing protein-1 (UBIAD1) is an enzyme catalyzing biosynthesis of coenzyme Q10 and vitamin K2.	coq	100-112	UbiA prenyltransferase domain containing 1	Homo sapiens	0-50
31634899-8	2019	We further demonstrate that ferroptosis suppression by FSP1 is mediated via ubiquinone (CoQ10): its reduced form ubiquinol traps lipid peroxyl radicals that mediate lipid peroxidation, while FSP1 catalyses its regeneration by using NAD(P)H.	coq	88-93	S100 calcium binding protein A4	Homo sapiens	55-59
31634899-10	2019	In conclusion, FSP1/CoQ10/NAD(P)H exists as a stand-alone parallel system, which co-operates with GPX4 and glutathione (GSH) to suppress phospholipid peroxidation (pLPO) and ferroptosis.	coq	20-25	S100 calcium binding protein A4	Homo sapiens	15-19
31737205-5	2019	Our results showed that CoQ10 treatment could significantly decrease the levels of oxidative products (MDA) and increase the activities of antioxidant enzymes (SOD and GSH) against oxidative stress, as well as decrease the levels of pro-apoptotic proteins (Bax and Caspase-3) and increase the levels of anti-apoptotic proteins (Bcl-2) against apoptosis after SCI.	coq	24-29	BCL2 associated X, apoptosis regulator	Rattus norvegicus	257-260
31737205-5	2019	Our results showed that CoQ10 treatment could significantly decrease the levels of oxidative products (MDA) and increase the activities of antioxidant enzymes (SOD and GSH) against oxidative stress, as well as decrease the levels of pro-apoptotic proteins (Bax and Caspase-3) and increase the levels of anti-apoptotic proteins (Bcl-2) against apoptosis after SCI.	coq	24-29	caspase 3	Rattus norvegicus	265-274
31737205-5	2019	Our results showed that CoQ10 treatment could significantly decrease the levels of oxidative products (MDA) and increase the activities of antioxidant enzymes (SOD and GSH) against oxidative stress, as well as decrease the levels of pro-apoptotic proteins (Bax and Caspase-3) and increase the levels of anti-apoptotic proteins (Bcl-2) against apoptosis after SCI.	coq	24-29	BCL2, apoptosis regulator	Rattus norvegicus	328-333
31737205-6	2019	We also observed that CoQ10 exerted beneficial effects through the Nrf-2/NQO-1 and NF-kappaB signaling pathway.	coq	22-27	NFE2 like bZIP transcription factor 2	Rattus norvegicus	67-72
31737205-6	2019	We also observed that CoQ10 exerted beneficial effects through the Nrf-2/NQO-1 and NF-kappaB signaling pathway.	coq	22-27	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	73-78
31185284-0	2019	Can coenzyme Q10 supplementation effectively reduce human tumor necrosis factor-alpha and interleukin-6 levels in chronic inflammatory diseases?	coq	4-16	tumor necrosis factor	Homo sapiens	58-85
31185284-0	2019	Can coenzyme Q10 supplementation effectively reduce human tumor necrosis factor-alpha and interleukin-6 levels in chronic inflammatory diseases?	coq	4-16	interleukin 6	Homo sapiens	90-103
31185284-5	2019	The objective of this systematic review and meta-analysis of randomized clinical trials (RCTs) was to assess the efficacy of CoQ10 supplementation on tumor necrosis factor- alpha (TNF-alpha) and interleukin-6 (IL-6) levels.	coq	125-130	tumor necrosis factor	Homo sapiens	150-178
31185284-5	2019	The objective of this systematic review and meta-analysis of randomized clinical trials (RCTs) was to assess the efficacy of CoQ10 supplementation on tumor necrosis factor- alpha (TNF-alpha) and interleukin-6 (IL-6) levels.	coq	125-130	tumor necrosis factor	Homo sapiens	180-189
31185284-5	2019	The objective of this systematic review and meta-analysis of randomized clinical trials (RCTs) was to assess the efficacy of CoQ10 supplementation on tumor necrosis factor- alpha (TNF-alpha) and interleukin-6 (IL-6) levels.	coq	125-130	interleukin 6	Homo sapiens	195-208
31185284-5	2019	The objective of this systematic review and meta-analysis of randomized clinical trials (RCTs) was to assess the efficacy of CoQ10 supplementation on tumor necrosis factor- alpha (TNF-alpha) and interleukin-6 (IL-6) levels.	coq	125-130	interleukin 6	Homo sapiens	210-214
31185284-12	2019	Our meta-analysis indicated that oral CoQ10 supplementation (60-500 mg/day for 8-12 weeks) resulted in significant reduction of TNF-alpha (SMD: -0.44, 95% CI: [-0.81 to -0.07] mg/dl; I2 = 66.1%, p  = 0.00) and IL-6 levels (SMD: -0.37, 95% CI: [-0.65 to -0.09]; I2 = 57.2, p  = 0.01), respectively.	coq	38-43	tumor necrosis factor	Homo sapiens	128-137
31185284-12	2019	Our meta-analysis indicated that oral CoQ10 supplementation (60-500 mg/day for 8-12 weeks) resulted in significant reduction of TNF-alpha (SMD: -0.44, 95% CI: [-0.81 to -0.07] mg/dl; I2 = 66.1%, p  = 0.00) and IL-6 levels (SMD: -0.37, 95% CI: [-0.65 to -0.09]; I2 = 57.2, p  = 0.01), respectively.	coq	38-43	interleukin 6	Homo sapiens	210-214
31582012-6	2019	Additionally, CoQ10 restored oxidant/antioxidant balance via marked activated Nrf-2 protein as well as up-regulation of both Sirt-1 and FOXO-3 genes.	coq	14-19	NFE2 like bZIP transcription factor 2	Rattus norvegicus	78-83
31582012-0	2019	Coenzyme Q10 protects hepatocytes from ischemia reperfusion-induced apoptosis and oxidative stress via regulation of Bax/Bcl-2/PUMA and Nrf-2/FOXO-3/Sirt-1 signaling pathways.	coq	0-12	BCL2 associated X, apoptosis regulator	Rattus norvegicus	117-120
31582012-0	2019	Coenzyme Q10 protects hepatocytes from ischemia reperfusion-induced apoptosis and oxidative stress via regulation of Bax/Bcl-2/PUMA and Nrf-2/FOXO-3/Sirt-1 signaling pathways.	coq	0-12	BCL2, apoptosis regulator	Rattus norvegicus	121-126
31582012-0	2019	Coenzyme Q10 protects hepatocytes from ischemia reperfusion-induced apoptosis and oxidative stress via regulation of Bax/Bcl-2/PUMA and Nrf-2/FOXO-3/Sirt-1 signaling pathways.	coq	0-12	Bcl-2 binding component 3	Rattus norvegicus	127-131
31582012-0	2019	Coenzyme Q10 protects hepatocytes from ischemia reperfusion-induced apoptosis and oxidative stress via regulation of Bax/Bcl-2/PUMA and Nrf-2/FOXO-3/Sirt-1 signaling pathways.	coq	0-12	NFE2 like bZIP transcription factor 2	Rattus norvegicus	136-141
31582012-0	2019	Coenzyme Q10 protects hepatocytes from ischemia reperfusion-induced apoptosis and oxidative stress via regulation of Bax/Bcl-2/PUMA and Nrf-2/FOXO-3/Sirt-1 signaling pathways.	coq	0-12	forkhead box O3	Rattus norvegicus	142-148
31582012-0	2019	Coenzyme Q10 protects hepatocytes from ischemia reperfusion-induced apoptosis and oxidative stress via regulation of Bax/Bcl-2/PUMA and Nrf-2/FOXO-3/Sirt-1 signaling pathways.	coq	0-12	sirtuin 1	Rattus norvegicus	149-155
31582012-6	2019	Additionally, CoQ10 restored oxidant/antioxidant balance via marked activated Nrf-2 protein as well as up-regulation of both Sirt-1 and FOXO-3 genes.	coq	14-19	sirtuin 1	Rattus norvegicus	125-131
31582012-6	2019	Additionally, CoQ10 restored oxidant/antioxidant balance via marked activated Nrf-2 protein as well as up-regulation of both Sirt-1 and FOXO-3 genes.	coq	14-19	forkhead box O3	Rattus norvegicus	136-142
31582012-7	2019	Moreover, CoQ10 strongly inhibited inflammatory response through down-regulation of NF-kappaB-p65 and decrease both JAK1 and STAT-3 protein expressions with a subsequent modulating circulating inflammatory cytokines.	coq	10-15	Janus kinase 1	Rattus norvegicus	116-120
31582012-7	2019	Moreover, CoQ10 strongly inhibited inflammatory response through down-regulation of NF-kappaB-p65 and decrease both JAK1 and STAT-3 protein expressions with a subsequent modulating circulating inflammatory cytokines.	coq	10-15	signal transducer and activator of transcription 3	Rattus norvegicus	125-131
32257901-4	2019	In the mRNA expression, there was a significant effect (P < 0.05) of the CoQ10 supplement on the mRNA expression of superoxide dismutase (SOD), although the mRNA expression of glutathione peroxidase (GPX) and glutathione S-transferase (GST) was unaffected by cholesterol or the CoQ10 supplement.	coq	73-78	hematopoietic prostaglandin D synthase	Rattus norvegicus	209-234
32257901-4	2019	In the mRNA expression, there was a significant effect (P < 0.05) of the CoQ10 supplement on the mRNA expression of superoxide dismutase (SOD), although the mRNA expression of glutathione peroxidase (GPX) and glutathione S-transferase (GST) was unaffected by cholesterol or the CoQ10 supplement.	coq	73-78	hematopoietic prostaglandin D synthase	Rattus norvegicus	236-239
31323021-2	2019	UbiA prenyltransferase domain-containing protein-1 (UBIAD1) is an enzyme catalyzing biosynthesis of coenzyme Q10 and vitamin K2.	coq	100-112	UbiA prenyltransferase domain containing 1	Homo sapiens	52-58
30881598-10	2019	A rescue experiment using specific inhibitors of the PI3K-AKT-mTOR pathway demonstrated that the PI3K-AKT-mTOR signaling pathway was the underlying mechanism by which CoQ10 ameliorated fibrosis.	coq	167-172	thymoma viral proto-oncogene 1	Mus musculus	58-61
30536661-4	2019	LDLr -/- mice were treated with pravastatin and/or CoQ 10 for 2 months.	coq	51-57	low density lipoprotein receptor	Mus musculus	0-4
30536661-8	2019	In vitro, insulin-secreting INS1E cells cotreated with CoQ 10 were protected from cell death and oxidative stress induced by pravastatin.	coq	55-61	insulin 1	Rattus norvegicus	28-32
30991050-0	2019	The in vitro and in vivo depigmenting activity of Coenzyme Q10 through the down-regulation of alpha-MSH signaling pathways and induction of Nrf2/ARE-mediated antioxidant genes in UVA-irradiated skin keratinocytes.	coq	50-62	STAM binding protein	Homo sapiens	94-103
30991050-0	2019	The in vitro and in vivo depigmenting activity of Coenzyme Q10 through the down-regulation of alpha-MSH signaling pathways and induction of Nrf2/ARE-mediated antioxidant genes in UVA-irradiated skin keratinocytes.	coq	50-62	NFE2 like bZIP transcription factor 2	Homo sapiens	140-144
30991050-4	2019	It was observed that CoQ10 suppressed p53/POMC, alpha-MSH production as well as inhibited ROS generation in UVA-irradiated keratinocyte HaCaT cells.	coq	21-26	tumor protein p53	Homo sapiens	38-41
30991050-4	2019	It was observed that CoQ10 suppressed p53/POMC, alpha-MSH production as well as inhibited ROS generation in UVA-irradiated keratinocyte HaCaT cells.	coq	21-26	proopiomelanocortin	Homo sapiens	42-46
30991050-4	2019	It was observed that CoQ10 suppressed p53/POMC, alpha-MSH production as well as inhibited ROS generation in UVA-irradiated keratinocyte HaCaT cells.	coq	21-26	STAM binding protein	Homo sapiens	48-57
30991050-5	2019	CoQ10 down-regulated the melanin synthesis in alpha-MSH-stimulated B16-F10 cells by suppressing the MITF expression by down regulating the cAMP mediated CREB signaling cascades.	coq	0-5	STAM binding protein	Mus musculus	46-55
30991050-5	2019	CoQ10 down-regulated the melanin synthesis in alpha-MSH-stimulated B16-F10 cells by suppressing the MITF expression by down regulating the cAMP mediated CREB signaling cascades.	coq	0-5	melanogenesis associated transcription factor	Mus musculus	100-104
30991050-5	2019	CoQ10 down-regulated the melanin synthesis in alpha-MSH-stimulated B16-F10 cells by suppressing the MITF expression by down regulating the cAMP mediated CREB signaling cascades.	coq	0-5	cAMP responsive element binding protein 1	Mus musculus	153-157
30991050-8	2019	Notably, silencing of Nrf2 (siRNA transfection) significantly diminished CoQ10-mediated anti-melanogenic activity, as evidenced by impaired antioxidant HO-1 gene, uncontrolled ROS generation, and alpha-MSH production following UVA irradiation.	coq	73-78	NFE2 like bZIP transcription factor 2	Homo sapiens	22-26
30991050-8	2019	Notably, silencing of Nrf2 (siRNA transfection) significantly diminished CoQ10-mediated anti-melanogenic activity, as evidenced by impaired antioxidant HO-1 gene, uncontrolled ROS generation, and alpha-MSH production following UVA irradiation.	coq	73-78	heme oxygenase 1	Homo sapiens	152-156
30991050-8	2019	Notably, silencing of Nrf2 (siRNA transfection) significantly diminished CoQ10-mediated anti-melanogenic activity, as evidenced by impaired antioxidant HO-1 gene, uncontrolled ROS generation, and alpha-MSH production following UVA irradiation.	coq	73-78	STAM binding protein	Homo sapiens	196-205
30847826-0	2019	COQ4 Mutation Leads to Childhood-Onset Ataxia Improved by CoQ10 Administration.	coq	58-63	coenzyme Q4	Homo sapiens	0-4
30737270-2	2019	We recently reported that individuals with mutations in COQ6, a coenzyme Q (also called CoQ10, CoQ, or ubiquinone) biosynthesis pathway enzyme, develop SRNS with sensorineural deafness, and demonstrated the beneficial effect of CoQ for maintenace of kidney function.	coq	88-93	coenzyme Q6 monooxygenase	Mus musculus	56-60
30721766-3	2019	In this study, we investigated the neuroprotective effects of Q10 on Abeta-induced impairment in hippocampal long-term potentiation (LTP), a widely researched model of synaptic plasticity, which occurs during learning and memory, in a rat model of AD.	coq	62-65	amyloid beta precursor protein	Rattus norvegicus	69-74
30721766-9	2019	Q10 treatment of Abeta-injected rats significantly attenuated these decreases, suggesting that Q10 reduces the effects of Abeta on LTP.	coq	0-3	amyloid beta precursor protein	Rattus norvegicus	17-22
30721766-9	2019	Q10 treatment of Abeta-injected rats significantly attenuated these decreases, suggesting that Q10 reduces the effects of Abeta on LTP.	coq	0-3	amyloid beta precursor protein	Rattus norvegicus	122-127
30721766-9	2019	Q10 treatment of Abeta-injected rats significantly attenuated these decreases, suggesting that Q10 reduces the effects of Abeta on LTP.	coq	95-98	amyloid beta precursor protein	Rattus norvegicus	17-22
30721766-9	2019	Q10 treatment of Abeta-injected rats significantly attenuated these decreases, suggesting that Q10 reduces the effects of Abeta on LTP.	coq	95-98	amyloid beta precursor protein	Rattus norvegicus	122-127
29228766-1	2019	BACKGROUND/AIMS: This study was performed to determine whether adding coenzyme Q10 (CoQ10) to metformin (MET) has a beneficial effect as a treatment for sirolimus (SRL)-induced diabetes mellitus (DM).	coq	70-82	MET proto-oncogene, receptor tyrosine kinase	Rattus norvegicus	105-108
29228766-6	2019	The addition of CoQ10 to MET further improved hyperglycemia, decreased HOMA-R index, and increased plasma insulin concentration compared with the SRL group than MET alone therapy.	coq	16-21	MET proto-oncogene, receptor tyrosine kinase	Rattus norvegicus	161-164
29228766-8	2019	In addition, co-treatment of CoQ10 and MET significantly increased the levels of antiperoxidative enzymes in the pancreas islet cells compared with MET.	coq	29-34	MET proto-oncogene, receptor tyrosine kinase	Rattus norvegicus	148-151
30668894-6	2019	METHODS AND RESULTS: Treatment with oral CoQ10 for 4 weeks abolished nicotinamide adenine dinucleotide phosphate-oxidase (NADPH oxidase) activation, decreased p38 phosphorylation, and increased superoxide dismutase 2 production in the NTS of fructose-fed rats.	coq	41-46	mitogen activated protein kinase 14	Rattus norvegicus	159-162
30668894-8	2019	Oral CoQ10 reduced blood pressure by inducing Akt and nNOS phosphorylation in NTS of fructose-induced hypertensive rats.	coq	5-10	AKT serine/threonine kinase 1	Rattus norvegicus	46-49
30668894-8	2019	Oral CoQ10 reduced blood pressure by inducing Akt and nNOS phosphorylation in NTS of fructose-induced hypertensive rats.	coq	5-10	nitric oxide synthase 1	Rattus norvegicus	54-58
30668894-9	2019	CONCLUSION: Oral CoQ10 decreases blood pressure by negatively regulating fructose-induced NADPH oxidase levels, abolishing ROS generation, reducing p38 phosphorylation, and enhancing the Akt-nNOS pathway in the NTS.	coq	17-22	mitogen activated protein kinase 14	Rattus norvegicus	148-151
30668894-9	2019	CONCLUSION: Oral CoQ10 decreases blood pressure by negatively regulating fructose-induced NADPH oxidase levels, abolishing ROS generation, reducing p38 phosphorylation, and enhancing the Akt-nNOS pathway in the NTS.	coq	17-22	AKT serine/threonine kinase 1	Rattus norvegicus	187-190
30668894-9	2019	CONCLUSION: Oral CoQ10 decreases blood pressure by negatively regulating fructose-induced NADPH oxidase levels, abolishing ROS generation, reducing p38 phosphorylation, and enhancing the Akt-nNOS pathway in the NTS.	coq	17-22	nitric oxide synthase 1	Rattus norvegicus	191-195
30881598-10	2019	A rescue experiment using specific inhibitors of the PI3K-AKT-mTOR pathway demonstrated that the PI3K-AKT-mTOR signaling pathway was the underlying mechanism by which CoQ10 ameliorated fibrosis.	coq	167-172	mechanistic target of rapamycin kinase	Mus musculus	62-66
30881598-10	2019	A rescue experiment using specific inhibitors of the PI3K-AKT-mTOR pathway demonstrated that the PI3K-AKT-mTOR signaling pathway was the underlying mechanism by which CoQ10 ameliorated fibrosis.	coq	167-172	thymoma viral proto-oncogene 1	Mus musculus	102-105
30881598-10	2019	A rescue experiment using specific inhibitors of the PI3K-AKT-mTOR pathway demonstrated that the PI3K-AKT-mTOR signaling pathway was the underlying mechanism by which CoQ10 ameliorated fibrosis.	coq	167-172	mechanistic target of rapamycin kinase	Mus musculus	106-110
30297204-6	2018	Furthermore, the extent of lipid peroxidation in thawed spermatozoa treated with 1 and 2 muM CoQ10 was less than with the other groups.	coq	93-98	latexin	Homo sapiens	89-92
30620716-8	2019	CoQ10-mediated renoprotective effects were abrogated by the Nrf2 inhibitor ML385.	coq	0-5	nuclear factor, erythroid derived 2, like 2	Mus musculus	60-64
30620716-10	2019	These results suggest that CoQ10, as an effective antioxidant in mitochondria, exerts beneficial effects in DN via mitophagy by restoring Nrf2/ARE signaling.	coq	27-32	nuclear factor, erythroid derived 2, like 2	Mus musculus	138-142
30393023-9	2019	ALA and/or CoQ10 treatment dramatically suppressed DN - induced oxidative stress which was associated with decrease in LPO and ROS and increase in GSH and TAC in DRG neurons.	coq	11-16	lactoperoxidase	Rattus norvegicus	119-122
30393023-10	2019	ALA and/or CoQ10 was proved to prevent apoptosis and degeneration of DRG neurons, which appears to be mediated by regulating the expression of caspase 3 and UCP2 proteins, inducing ATP and improving DN-induced changes in DRG neurons.	coq	11-16	caspase 3	Rattus norvegicus	143-152
30393023-10	2019	ALA and/or CoQ10 was proved to prevent apoptosis and degeneration of DRG neurons, which appears to be mediated by regulating the expression of caspase 3 and UCP2 proteins, inducing ATP and improving DN-induced changes in DRG neurons.	coq	11-16	uncoupling protein 2	Rattus norvegicus	157-161
31233687-15	2019	The biomarkers of the immunotropic effect of L-carnitine and coenzyme Q10 are a decrease in the expression of the apoptotic marker CD95/Fas on peripheral blood lymphocytes and suppression of the production of pro-inflammatory cytokines synthesized by Th1-lymphocytes with switching the response to humoral immunity.	coq	61-73	Fas cell surface death receptor	Homo sapiens	131-135
31349945-10	2019	Co-Q10 and vitamin E (alone or in combination) had significant effects on non-HDL-C (p = 0.004), atherogenic Index of Plasma (AIP) (p = &lt;0.001) and lipid accumulation product (LAP) (p &lt;0.001) and SBP (p = 0.005).	coq	0-6	aryl hydrocarbon receptor interacting protein	Homo sapiens	97-130
31349945-10	2019	Co-Q10 and vitamin E (alone or in combination) had significant effects on non-HDL-C (p = 0.004), atherogenic Index of Plasma (AIP) (p = &lt;0.001) and lipid accumulation product (LAP) (p &lt;0.001) and SBP (p = 0.005).	coq	0-6	selenium binding protein 1	Homo sapiens	202-205
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	coq	25-30	mechanistic target of rapamycin kinase	Homo sapiens	203-232
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	coq	25-30	RAR related orphan receptor C	Homo sapiens	236-239
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	coq	25-30	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	242-294
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	coq	25-30	microtubule associated protein 1 light chain 3 beta	Homo sapiens	296-304
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	coq	25-30	sequestosome 1	Homo sapiens	352-355
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	coq	25-30	sequestosome 1	Homo sapiens	357-360
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	coq	25-30	sequestosome 1	Homo sapiens	361-367
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	coq	25-30	high mobility group box 1	Homo sapiens	401-431
30551543-5	2019	Concomitant treatment of CoQ10 &amp; methotrexate caused improvement in histological picture of the lung and liver tissues, liver function and oxidative stress biomarkers, modulation of autophagy genes [mammalian target of rapamycin (m-TOR), Microtubule-associated proteins 1 A/1B light chain 3 (MAP1LC3B), and Sequestosome 1 ubiquitin-binding protein p62 (p62/SQSTM1)] with simultaneous reduction in High Mobility Group Protein B1 (HMGB1).	coq	25-30	high mobility group box 1	Homo sapiens	433-438
31187715-4	2019	Coenzyme Q10 (CoQ10), as a part of the mitochondrial respiratory chain can effectively restore these neuronal dysfunctions by preventing the opening of mitochondrial membrane transition pore, thereby counteracting cell death events as well as exerts an anti-inflammatory effect by influencing the expression of NF-kB1 dependent genes thus preventing the neuroinflammation and energy restoration.	coq	0-12	nuclear factor kappa B subunit 1	Homo sapiens	311-317
31187715-4	2019	Coenzyme Q10 (CoQ10), as a part of the mitochondrial respiratory chain can effectively restore these neuronal dysfunctions by preventing the opening of mitochondrial membrane transition pore, thereby counteracting cell death events as well as exerts an anti-inflammatory effect by influencing the expression of NF-kB1 dependent genes thus preventing the neuroinflammation and energy restoration.	coq	14-19	nuclear factor kappa B subunit 1	Homo sapiens	311-317
30003820-5	2018	Our aim is to investigate the effectiveness of CoQ10 in serving in the ETF/ETFDH system to improve mitochondrial function and to reduce lipotoxicity.	coq	47-52	electron transfer flavoprotein dehydrogenase	Homo sapiens	75-80
30003820-8	2018	In contrast, supplementation with CoQ10 significantly recovered mitochondrial function and concurrently decreased the generation of reactive oxygen species and lipid peroxides, inhibited the accumulation of lipid droplets and the formation of the NOD-like receptor family pyrin domain-containing three (NLRP3) inflammasome, and reduced interleukin-1beta release and cell death.	coq	34-39	NLR family pyrin domain containing 3	Homo sapiens	303-308
30003820-8	2018	In contrast, supplementation with CoQ10 significantly recovered mitochondrial function and concurrently decreased the generation of reactive oxygen species and lipid peroxides, inhibited the accumulation of lipid droplets and the formation of the NOD-like receptor family pyrin domain-containing three (NLRP3) inflammasome, and reduced interleukin-1beta release and cell death.	coq	34-39	interleukin 1 beta	Homo sapiens	336-353
30261465-0	2018	Potential therapeutic role of Co-Q10 in alleviating intervertebral disc degeneration and suppressing IL-1beta-mediated inflammatory reaction in NP cells.	coq	30-36	interleukin 1 beta	Homo sapiens	101-109
29577973-3	2018	In animal models, coenzyme Q10 (CoQ) also attenuates inflammation by reducing MPO and LTB4.	coq	32-35	myeloperoxidase	Homo sapiens	78-81
30116167-8	2018	N-acetyl cysteine and/or CoQ10 significantly decreased hydroxyproline level compared to that of CCl4-treated rats.	coq	25-30	C-C motif chemokine ligand 4	Rattus norvegicus	96-100
29784452-9	2018	RESULTS: CoQ did not affect oxygen consumption but reduced the level of O2- and H2O2 while shifted to a pro-oxidant cell status mainly due to a decrease in catalase activity and SOD2 level.	coq	9-12	immunoglobulin kappa variable 1D-39	Homo sapiens	72-84
29784452-9	2018	RESULTS: CoQ did not affect oxygen consumption but reduced the level of O2- and H2O2 while shifted to a pro-oxidant cell status mainly due to a decrease in catalase activity and SOD2 level.	coq	9-12	superoxide dismutase 2	Homo sapiens	178-182
30261465-6	2018	Levels of IL-1beta-induced inflammatory biomarkers including TNF-alpha, COX-2, IL-6 and iNOS were reduced by Co-Q10, which was possibly associated with inhibition of NF-kappaB signaling activation.	coq	109-115	interleukin 1 beta	Homo sapiens	10-18
30261465-6	2018	Levels of IL-1beta-induced inflammatory biomarkers including TNF-alpha, COX-2, IL-6 and iNOS were reduced by Co-Q10, which was possibly associated with inhibition of NF-kappaB signaling activation.	coq	109-115	tumor necrosis factor	Homo sapiens	61-70
30261465-6	2018	Levels of IL-1beta-induced inflammatory biomarkers including TNF-alpha, COX-2, IL-6 and iNOS were reduced by Co-Q10, which was possibly associated with inhibition of NF-kappaB signaling activation.	coq	109-115	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	72-77
30261465-6	2018	Levels of IL-1beta-induced inflammatory biomarkers including TNF-alpha, COX-2, IL-6 and iNOS were reduced by Co-Q10, which was possibly associated with inhibition of NF-kappaB signaling activation.	coq	109-115	interleukin 6	Homo sapiens	79-83
30261465-7	2018	Furthermore, Co-Q10 maintained the production of anabolic biomarkers in NP cells such as collagen 2, aggrecan and Sox-9 and altered the enhanced catabolism induced by IL-1beta.	coq	13-19	SRY-box transcription factor 9	Homo sapiens	114-119
30261465-7	2018	Furthermore, Co-Q10 maintained the production of anabolic biomarkers in NP cells such as collagen 2, aggrecan and Sox-9 and altered the enhanced catabolism induced by IL-1beta.	coq	13-19	interleukin 1 beta	Homo sapiens	167-175
29663377-3	2018	Recently, analysis of UBIAD1 has indicated it is a prenyltransferase enzyme for both non-mitochondrial CoQ10 and vitamin K2 production.	coq	103-108	UbiA prenyltransferase domain containing 1	Mus musculus	22-28
29997512-10	2018	Diet supplementation with the antioxidants CoQ10 or creatine fully reversed all pravastatin effects (reduced H2O2 generation, susceptibility to MPT and normalized aconitase and G6PD activity).	coq	43-48	glucose-6-phosphate dehydrogenase 2	Mus musculus	177-181
29291430-5	2018	We investigated the role of these 5-HT receptors and their linked GSK-3beta signaling intermediates as an underlying mechanism of CoQ10 as monotherapy or combined with fluoxetine, a selective serotonin reuptake inhibitor, to alleviate depressive-like phenotype.	coq	130-135	glycogen synthase kinase 3 beta	Rattus norvegicus	66-75
29080629-2	2018	Mutations in COQ2, an enzyme involved in coenzyme Q10 synthesis, were recently associated with familial and sporadic cases of multiple-system atrophy.	coq	41-53	coenzyme Q2, polyprenyltransferase	Homo sapiens	13-17
30417782-9	2018	CONCLUSION: Overall, the current meta-analysis demonstrated that CoQ10 supplementation significantly improved metabolic profile in patients with CKD by reducing total cholesterol, LDL-cholesterol, MDA and creatinine levels, yet it did not affect fasting glucose, insulin, HOMA-IR, and CRP concentrations.	coq	65-70	insulin	Homo sapiens	263-270
30417782-9	2018	CONCLUSION: Overall, the current meta-analysis demonstrated that CoQ10 supplementation significantly improved metabolic profile in patients with CKD by reducing total cholesterol, LDL-cholesterol, MDA and creatinine levels, yet it did not affect fasting glucose, insulin, HOMA-IR, and CRP concentrations.	coq	65-70	C-reactive protein	Homo sapiens	285-288
29107645-1	2018	INTRODUCTION: The finding of mutations of the COQ2 gene and reduced coenzyme Q10 levels in the cerebellum in multiple system atrophy (MSA) suggest that coenzyme Q10 is relevant to MSA pathophysiology.	coq	152-164	coenzyme Q2, polyprenyltransferase	Homo sapiens	46-50
29115467-14	2018	The above effects of CoQ10 may be mediated by activation of the PTEN/PI3K/AKT pathway.	coq	21-26	phosphatase and tensin homolog	Rattus norvegicus	64-68
29115467-14	2018	The above effects of CoQ10 may be mediated by activation of the PTEN/PI3K/AKT pathway.	coq	21-26	AKT serine/threonine kinase 1	Rattus norvegicus	74-77
29190916-11	2017	Conclusions: Our finding suggests that CoQ10 inhibits the activation of PSCs by suppressing autophagy through activating the PI3K/AKT/mTOR signaling pathway.	coq	39-44	thymoma viral proto-oncogene 1	Mus musculus	130-133
29081748-0	2017	CoQ10 Augments Rosuvastatin Neuroprotective Effect in a Model of Global Ischemia via Inhibition of NF-kappaB/JNK3/Bax and Activation of Akt/FOXO3A/Bim Cues.	coq	0-5	mitogen activated protein kinase 10	Rattus norvegicus	109-113
29081748-0	2017	CoQ10 Augments Rosuvastatin Neuroprotective Effect in a Model of Global Ischemia via Inhibition of NF-kappaB/JNK3/Bax and Activation of Akt/FOXO3A/Bim Cues.	coq	0-5	BCL2 associated X, apoptosis regulator	Rattus norvegicus	114-117
29081748-0	2017	CoQ10 Augments Rosuvastatin Neuroprotective Effect in a Model of Global Ischemia via Inhibition of NF-kappaB/JNK3/Bax and Activation of Akt/FOXO3A/Bim Cues.	coq	0-5	AKT serine/threonine kinase 1	Rattus norvegicus	136-139
29081748-0	2017	CoQ10 Augments Rosuvastatin Neuroprotective Effect in a Model of Global Ischemia via Inhibition of NF-kappaB/JNK3/Bax and Activation of Akt/FOXO3A/Bim Cues.	coq	0-5	forkhead box O3	Rattus norvegicus	140-146
29081748-0	2017	CoQ10 Augments Rosuvastatin Neuroprotective Effect in a Model of Global Ischemia via Inhibition of NF-kappaB/JNK3/Bax and Activation of Akt/FOXO3A/Bim Cues.	coq	0-5	Bcl2-like 11	Rattus norvegicus	147-150
29190916-11	2017	Conclusions: Our finding suggests that CoQ10 inhibits the activation of PSCs by suppressing autophagy through activating the PI3K/AKT/mTOR signaling pathway.	coq	39-44	mechanistic target of rapamycin kinase	Mus musculus	134-138
27335030-7	2017	Interestingly, complexin-1/2, two molecules which were shown to alter LTP, were modulated (i.e., the levels were reduced in 3xTg-AD mice and CoQ10 restored the levels) in response to CoQ10 treatment among these nine proteins.	coq	141-146	complexin 1	Mus musculus	15-28
27335030-7	2017	Interestingly, complexin-1/2, two molecules which were shown to alter LTP, were modulated (i.e., the levels were reduced in 3xTg-AD mice and CoQ10 restored the levels) in response to CoQ10 treatment among these nine proteins.	coq	183-188	complexin 1	Mus musculus	15-28
27335030-10	2017	The modulation of complexin-1/2 expression by CoQ10 may contribute to the amelioration of memory impairment in the AD transgenic mice.	coq	46-51	complexin 1	Mus musculus	18-31
28263872-2	2017	We show increased oxidative stress, abnormalities in the antioxidant system, changes in complexes involved in oxidative phosphorylation and changes in mitochondrial morphology in SCA2 patient fibroblasts compared to controls, and we show that treatment with CoQ10 can partially reverse these changes.	coq	258-263	ataxin 2	Homo sapiens	179-183
28458038-5	2017	CoQ10 suppressed the protein expression of COX-2 and the level of PGE2 in Abeta25-35-injured PC12 cells.	coq	0-5	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	43-48
28410798-6	2017	CoQ10 or L-carnitine showed a noticeable effects in improving cardiac functions evidenced reducing serum enzymes as serum interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), leptin, lactate dehydrogenase (LDH), Cardiotrophin-1, Troponin-I and Troponin-T. Also, alleviate oxidative stress, decrease of cardiac Malondialdehyde (MDA), Nitric oxide (NO) and restoring cardiac reduced glutathione levels to normal levels.	coq	0-5	interleukin 1 beta	Rattus norvegicus	122-140
28410798-6	2017	CoQ10 or L-carnitine showed a noticeable effects in improving cardiac functions evidenced reducing serum enzymes as serum interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), leptin, lactate dehydrogenase (LDH), Cardiotrophin-1, Troponin-I and Troponin-T. Also, alleviate oxidative stress, decrease of cardiac Malondialdehyde (MDA), Nitric oxide (NO) and restoring cardiac reduced glutathione levels to normal levels.	coq	0-5	interleukin 1 beta	Rattus norvegicus	142-151
28410798-6	2017	CoQ10 or L-carnitine showed a noticeable effects in improving cardiac functions evidenced reducing serum enzymes as serum interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), leptin, lactate dehydrogenase (LDH), Cardiotrophin-1, Troponin-I and Troponin-T. Also, alleviate oxidative stress, decrease of cardiac Malondialdehyde (MDA), Nitric oxide (NO) and restoring cardiac reduced glutathione levels to normal levels.	coq	0-5	tumor necrosis factor	Rattus norvegicus	154-181
28410798-6	2017	CoQ10 or L-carnitine showed a noticeable effects in improving cardiac functions evidenced reducing serum enzymes as serum interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), leptin, lactate dehydrogenase (LDH), Cardiotrophin-1, Troponin-I and Troponin-T. Also, alleviate oxidative stress, decrease of cardiac Malondialdehyde (MDA), Nitric oxide (NO) and restoring cardiac reduced glutathione levels to normal levels.	coq	0-5	tumor necrosis factor	Rattus norvegicus	183-192
28410798-6	2017	CoQ10 or L-carnitine showed a noticeable effects in improving cardiac functions evidenced reducing serum enzymes as serum interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), leptin, lactate dehydrogenase (LDH), Cardiotrophin-1, Troponin-I and Troponin-T. Also, alleviate oxidative stress, decrease of cardiac Malondialdehyde (MDA), Nitric oxide (NO) and restoring cardiac reduced glutathione levels to normal levels.	coq	0-5	leptin	Rattus norvegicus	195-201
28410798-6	2017	CoQ10 or L-carnitine showed a noticeable effects in improving cardiac functions evidenced reducing serum enzymes as serum interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), leptin, lactate dehydrogenase (LDH), Cardiotrophin-1, Troponin-I and Troponin-T. Also, alleviate oxidative stress, decrease of cardiac Malondialdehyde (MDA), Nitric oxide (NO) and restoring cardiac reduced glutathione levels to normal levels.	coq	0-5	cardiotrophin 1	Rattus norvegicus	232-247
28190227-6	2017	Water-soluble CoQ10 prevented mitochondrial dynamic imbalance by reducing Drp1 and Fis1 protein expression to pre-rotenone levels, as well as reducing rotenone treatment-associated mitochondrial fragmentation.	coq	14-19	collapsin response mediator protein 1	Mus musculus	74-78
28190227-6	2017	Water-soluble CoQ10 prevented mitochondrial dynamic imbalance by reducing Drp1 and Fis1 protein expression to pre-rotenone levels, as well as reducing rotenone treatment-associated mitochondrial fragmentation.	coq	14-19	fission, mitochondrial 1	Mus musculus	83-87
28149310-5	2016	RESULTS: Compared with the placebo, CoQ10 intake led to a significant reduction in serum interleukin 6 (IL-6) (-1.7 +- 1.6 vs. 0.8 +- 1.7 ng/l, P &lt; 0.001) and protein carbonyl (PCO) levels (-0.2 +- 0.3 vs. 0.1 +- 0.2 nmol/mg protein, P &lt; 0.001).	coq	36-41	interleukin 6	Homo sapiens	89-102
28099869-6	2017	CoQ decreased levels were associated with down-regulation of the expression of COQ4 gene, as well as decreased Coq4 and Coq6 protein levels.	coq	0-3	coenzyme Q4	Homo sapiens	79-83
28099869-6	2017	CoQ decreased levels were associated with down-regulation of the expression of COQ4 gene, as well as decreased Coq4 and Coq6 protein levels.	coq	0-3	coenzyme Q4	Homo sapiens	111-115
28099869-6	2017	CoQ decreased levels were associated with down-regulation of the expression of COQ4 gene, as well as decreased Coq4 and Coq6 protein levels.	coq	0-3	coenzyme Q6, monooxygenase	Homo sapiens	120-124
27878228-5	2016	Here, we report on the potential use of lithium carbonate and coenzyme Q10 to reduce cell death caused by the expanded ATX3 in cell culture.	coq	62-74	ataxin 3	Homo sapiens	119-123
27878228-7	2016	Treatment with lithium carbonate and coenzyme Q10 led to a significant increase in viability of cells expressing expanded ATX3 (Q84).	coq	37-49	ataxin 3	Homo sapiens	122-126
27878228-9	2016	Furthermore, there was a significant change in the expanded ATX3 monomer/aggregate ratio after lithium carbonate and coenzyme Q10 treatment, with an increase in the monomer fraction and decrease in aggregates.	coq	117-129	ataxin 3	Homo sapiens	60-64
27143639-5	2016	The administration of exogenous water-soluble CoQ10 to aged mice via drinking water restored the mitochondrial OCR, motor function, and phosphorylated alpha-syn and VGluT1 levels in the motor cortex.	coq	46-51	synuclein, alpha	Mus musculus	151-160
27143639-5	2016	The administration of exogenous water-soluble CoQ10 to aged mice via drinking water restored the mitochondrial OCR, motor function, and phosphorylated alpha-syn and VGluT1 levels in the motor cortex.	coq	46-51	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 7	Mus musculus	165-171
27143639-6	2016	These results suggest that early-onset motor impairment and the increased accumulation of Ser129-phosphorylated alpha-syn in the motor cortex are ameliorated by the exogenous administration of CoQ10.	coq	193-198	synuclein, alpha	Mus musculus	112-121
27356913-2	2016	It has recently been reported that functionally impaired variants of COQ2, which encodes an essential enzyme in the biosynthetic pathway of coenzyme Q10 (CoQ10), are associated with MSA.	coq	140-152	coenzyme Q2, polyprenyltransferase	Homo sapiens	69-73
27356913-2	2016	It has recently been reported that functionally impaired variants of COQ2, which encodes an essential enzyme in the biosynthetic pathway of coenzyme Q10 (CoQ10), are associated with MSA.	coq	154-159	coenzyme Q2, polyprenyltransferase	Homo sapiens	69-73
28149310-5	2016	RESULTS: Compared with the placebo, CoQ10 intake led to a significant reduction in serum interleukin 6 (IL-6) (-1.7 +- 1.6 vs. 0.8 +- 1.7 ng/l, P &lt; 0.001) and protein carbonyl (PCO) levels (-0.2 +- 0.3 vs. 0.1 +- 0.2 nmol/mg protein, P &lt; 0.001).	coq	36-41	interleukin 6	Homo sapiens	104-108
27235405-1	2016	In familial and sporadic multiple system atrophy (MSA) patients, deficiency of coenzyme Q10 (CoQ10) has been associated with mutations in COQ2, which encodes the second enzyme in the CoQ10 biosynthetic pathway.	coq	79-91	coenzyme Q2, polyprenyltransferase	Homo sapiens	138-142
27544369-10	2016	SMDs for the effect of Co-Q10 on HbA1c and fasting insulin were -0.05% (95% CI: -0.22, 0.12) and 0.12 pmol/L (95% CI: -0.21, 0.44), respectively.	coq	23-29	insulin	Homo sapiens	51-58
27235405-1	2016	In familial and sporadic multiple system atrophy (MSA) patients, deficiency of coenzyme Q10 (CoQ10) has been associated with mutations in COQ2, which encodes the second enzyme in the CoQ10 biosynthetic pathway.	coq	93-98	coenzyme Q2, polyprenyltransferase	Homo sapiens	138-142
26682233-9	2016	Furthermore, treatment with CoQ10 reduced reactive oxygen species, enhanced eNOS/Akt activity, and increased HO-1 expression in high glucose-treated EPCs.	coq	28-33	nitric oxide synthase 3	Homo sapiens	76-80
26156412-7	2016	RESULTS: Taking 100 mg CoQ10 supplement daily resulted in a significant decrease in liver aminotransferases (aspartate aminotransferase [AST] and gamma-glutamyl transpeptidase [GGT]), high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor alpha, and the grades of NAFLD in the CoQ10 group in comparison to the control group (p &lt; 0.05).	coq	23-28	solute carrier family 17 member 5	Homo sapiens	109-135
26156412-7	2016	RESULTS: Taking 100 mg CoQ10 supplement daily resulted in a significant decrease in liver aminotransferases (aspartate aminotransferase [AST] and gamma-glutamyl transpeptidase [GGT]), high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor alpha, and the grades of NAFLD in the CoQ10 group in comparison to the control group (p &lt; 0.05).	coq	23-28	solute carrier family 17 member 5	Homo sapiens	137-140
26156412-7	2016	RESULTS: Taking 100 mg CoQ10 supplement daily resulted in a significant decrease in liver aminotransferases (aspartate aminotransferase [AST] and gamma-glutamyl transpeptidase [GGT]), high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor alpha, and the grades of NAFLD in the CoQ10 group in comparison to the control group (p &lt; 0.05).	coq	23-28	inactive glutathione hydrolase 2	Homo sapiens	146-175
26156412-7	2016	RESULTS: Taking 100 mg CoQ10 supplement daily resulted in a significant decrease in liver aminotransferases (aspartate aminotransferase [AST] and gamma-glutamyl transpeptidase [GGT]), high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor alpha, and the grades of NAFLD in the CoQ10 group in comparison to the control group (p &lt; 0.05).	coq	23-28	tumor necrosis factor	Homo sapiens	221-257
27374290-6	2016	In our study, Co-Q10 showed potent anti-oxidant and anti-inflammatory activities through a significant increase in catalase activity and glutathione content.	coq	14-20	catalase	Rattus norvegicus	115-123
26072159-10	2016	These findings suggest CoQ10 augments cellular antioxidant defense capacity through both intrinsic free radical-scavenging activity and activation of Nrf2 and subsequently antioxidant enzymes induction, thereby protecting the PC12 cells from H2O2-induced oxidative cytotoxicity.	coq	23-28	NFE2 like bZIP transcription factor 2	Rattus norvegicus	150-154
26341816-2	2016	Recently, Co-Q10 was reported to antagonize TNF-alpha-induced inflammation and play a protective role in various inflammatory conditions.	coq	10-16	tumor necrosis factor	Mus musculus	44-53
26341816-4	2016	Herein, RAW264.7 macrophage cell line was cultured with stimulation of TNF-alpha, and administration of Co-Q10 alleviated TNF-alpha-mediated inflammatory reaction in vitro.	coq	104-110	tumor necrosis factor	Mus musculus	71-80
26341816-4	2016	Herein, RAW264.7 macrophage cell line was cultured with stimulation of TNF-alpha, and administration of Co-Q10 alleviated TNF-alpha-mediated inflammatory reaction in vitro.	coq	104-110	tumor necrosis factor	Mus musculus	122-131
26812605-1	2016	The COQ2 gene encodes an essential enzyme for biogenesis, coenzyme Q10 (CoQ10).	coq	58-70	coenzyme Q2, polyprenyltransferase	Homo sapiens	4-8
26812605-1	2016	The COQ2 gene encodes an essential enzyme for biogenesis, coenzyme Q10 (CoQ10).	coq	72-77	coenzyme Q2, polyprenyltransferase	Homo sapiens	4-8
26682233-9	2016	Furthermore, treatment with CoQ10 reduced reactive oxygen species, enhanced eNOS/Akt activity, and increased HO-1 expression in high glucose-treated EPCs.	coq	28-33	AKT serine/threonine kinase 1	Homo sapiens	81-84
27047809-4	2016	OBJECTIVES: Due to increasing oxidative stress in dialysis patients, and the effect of CO-Q10 in decrease oxidative stress, in this work, we assessed the effect of CO-Q10 on C-reactive protein (CRP) level as an inflammatory marker and homocysteine in dialysis patients.	coq	87-93	C-reactive protein	Homo sapiens	174-192
27047809-4	2016	OBJECTIVES: Due to increasing oxidative stress in dialysis patients, and the effect of CO-Q10 in decrease oxidative stress, in this work, we assessed the effect of CO-Q10 on C-reactive protein (CRP) level as an inflammatory marker and homocysteine in dialysis patients.	coq	164-170	C-reactive protein	Homo sapiens	174-192
27047809-4	2016	OBJECTIVES: Due to increasing oxidative stress in dialysis patients, and the effect of CO-Q10 in decrease oxidative stress, in this work, we assessed the effect of CO-Q10 on C-reactive protein (CRP) level as an inflammatory marker and homocysteine in dialysis patients.	coq	164-170	C-reactive protein	Homo sapiens	194-197
27047809-10	2016	The treatment effect of CO-Q10 on CRP level is significant (P &lt; 0.001) (95% CI = -20.1 to -10.5) and it was also significant for the increasing albumin level.	coq	24-30	C-reactive protein	Homo sapiens	34-37
27047809-13	2016	CONCLUSIONS: CO-Q10 could significantly decrease CRP level as an inflammatory marker and can protect cardiovascular events.	coq	13-19	C-reactive protein	Homo sapiens	49-52
26410779-5	2015	The analysis of pro-inflammatory cytokines release by ELISA revealed that resveratrol, lipoic acid melatonin and Co-Q10 inhibited the BBB endothelial release of pro-inflammatory cytokines IL-6 and IL-8, reduced (not Co-Q10) CSE-induced up-regulation of Platelet Cell Adhesion Molecule-1 (PECAM-1), Vascular Cell Adhesion Molecule-1 (VCAM-1) &amp; E-selectin and inhibited monocytes-endothelial cell adhesion.	coq	113-119	interleukin 6	Homo sapiens	188-192
26205433-7	2016	Chi-square test showed a significant association between the fact of having low plasma PLP and CoQ values in the whole cohort of patients.	coq	95-98	pyridoxal phosphatase	Homo sapiens	87-90
26410779-5	2015	The analysis of pro-inflammatory cytokines release by ELISA revealed that resveratrol, lipoic acid melatonin and Co-Q10 inhibited the BBB endothelial release of pro-inflammatory cytokines IL-6 and IL-8, reduced (not Co-Q10) CSE-induced up-regulation of Platelet Cell Adhesion Molecule-1 (PECAM-1), Vascular Cell Adhesion Molecule-1 (VCAM-1) &amp; E-selectin and inhibited monocytes-endothelial cell adhesion.	coq	113-119	C-X-C motif chemokine ligand 8	Homo sapiens	197-201
26410779-5	2015	The analysis of pro-inflammatory cytokines release by ELISA revealed that resveratrol, lipoic acid melatonin and Co-Q10 inhibited the BBB endothelial release of pro-inflammatory cytokines IL-6 and IL-8, reduced (not Co-Q10) CSE-induced up-regulation of Platelet Cell Adhesion Molecule-1 (PECAM-1), Vascular Cell Adhesion Molecule-1 (VCAM-1) &amp; E-selectin and inhibited monocytes-endothelial cell adhesion.	coq	113-119	cell adhesion molecule 1	Homo sapiens	262-286
26410779-5	2015	The analysis of pro-inflammatory cytokines release by ELISA revealed that resveratrol, lipoic acid melatonin and Co-Q10 inhibited the BBB endothelial release of pro-inflammatory cytokines IL-6 and IL-8, reduced (not Co-Q10) CSE-induced up-regulation of Platelet Cell Adhesion Molecule-1 (PECAM-1), Vascular Cell Adhesion Molecule-1 (VCAM-1) &amp; E-selectin and inhibited monocytes-endothelial cell adhesion.	coq	113-119	platelet and endothelial cell adhesion molecule 1	Homo sapiens	288-295
26410779-5	2015	The analysis of pro-inflammatory cytokines release by ELISA revealed that resveratrol, lipoic acid melatonin and Co-Q10 inhibited the BBB endothelial release of pro-inflammatory cytokines IL-6 and IL-8, reduced (not Co-Q10) CSE-induced up-regulation of Platelet Cell Adhesion Molecule-1 (PECAM-1), Vascular Cell Adhesion Molecule-1 (VCAM-1) &amp; E-selectin and inhibited monocytes-endothelial cell adhesion.	coq	113-119	vascular cell adhesion molecule 1	Homo sapiens	298-331
26410779-5	2015	The analysis of pro-inflammatory cytokines release by ELISA revealed that resveratrol, lipoic acid melatonin and Co-Q10 inhibited the BBB endothelial release of pro-inflammatory cytokines IL-6 and IL-8, reduced (not Co-Q10) CSE-induced up-regulation of Platelet Cell Adhesion Molecule-1 (PECAM-1), Vascular Cell Adhesion Molecule-1 (VCAM-1) &amp; E-selectin and inhibited monocytes-endothelial cell adhesion.	coq	113-119	vascular cell adhesion molecule 1	Homo sapiens	333-339
26410779-5	2015	The analysis of pro-inflammatory cytokines release by ELISA revealed that resveratrol, lipoic acid melatonin and Co-Q10 inhibited the BBB endothelial release of pro-inflammatory cytokines IL-6 and IL-8, reduced (not Co-Q10) CSE-induced up-regulation of Platelet Cell Adhesion Molecule-1 (PECAM-1), Vascular Cell Adhesion Molecule-1 (VCAM-1) &amp; E-selectin and inhibited monocytes-endothelial cell adhesion.	coq	113-119	selectin E	Homo sapiens	347-357
26617520-8	2015	Treatment with CoQ10 (20 and 40 mg/kg) and minocycline (50 and 100 mg/kg) alone for 21 days significantly improved cognitive performance as evidenced by reduced transfer latency and increased time spent in target quadrant (TSTQ), reduced AChE activity, oxidative damage (reduced LPO, nitrite level and restored SOD, catalase and GHS levels), TNF-alpha level, restored mitochondrial respiratory enzyme complex (I, II, III, IV) activities and histopathological alterations as compared to Abeta (1-42) treated animals.	coq	15-20	acetylcholinesterase (Cartwright blood group)	Homo sapiens	238-242
26617520-8	2015	Treatment with CoQ10 (20 and 40 mg/kg) and minocycline (50 and 100 mg/kg) alone for 21 days significantly improved cognitive performance as evidenced by reduced transfer latency and increased time spent in target quadrant (TSTQ), reduced AChE activity, oxidative damage (reduced LPO, nitrite level and restored SOD, catalase and GHS levels), TNF-alpha level, restored mitochondrial respiratory enzyme complex (I, II, III, IV) activities and histopathological alterations as compared to Abeta (1-42) treated animals.	coq	15-20	lactoperoxidase	Homo sapiens	279-282
26522469-6	2015	We show that SLC25A26 mutations cause various mitochondrial defects, including those affecting RNA stability, protein modification, mitochondrial translation, and the biosynthesis of CoQ10 and lipoic acid.	coq	183-188	solute carrier family 25 member 26	Homo sapiens	13-21
26617520-8	2015	Treatment with CoQ10 (20 and 40 mg/kg) and minocycline (50 and 100 mg/kg) alone for 21 days significantly improved cognitive performance as evidenced by reduced transfer latency and increased time spent in target quadrant (TSTQ), reduced AChE activity, oxidative damage (reduced LPO, nitrite level and restored SOD, catalase and GHS levels), TNF-alpha level, restored mitochondrial respiratory enzyme complex (I, II, III, IV) activities and histopathological alterations as compared to Abeta (1-42) treated animals.	coq	15-20	catalase	Homo sapiens	316-324
26617520-8	2015	Treatment with CoQ10 (20 and 40 mg/kg) and minocycline (50 and 100 mg/kg) alone for 21 days significantly improved cognitive performance as evidenced by reduced transfer latency and increased time spent in target quadrant (TSTQ), reduced AChE activity, oxidative damage (reduced LPO, nitrite level and restored SOD, catalase and GHS levels), TNF-alpha level, restored mitochondrial respiratory enzyme complex (I, II, III, IV) activities and histopathological alterations as compared to Abeta (1-42) treated animals.	coq	15-20	GHS	Homo sapiens	329-332
26617520-8	2015	Treatment with CoQ10 (20 and 40 mg/kg) and minocycline (50 and 100 mg/kg) alone for 21 days significantly improved cognitive performance as evidenced by reduced transfer latency and increased time spent in target quadrant (TSTQ), reduced AChE activity, oxidative damage (reduced LPO, nitrite level and restored SOD, catalase and GHS levels), TNF-alpha level, restored mitochondrial respiratory enzyme complex (I, II, III, IV) activities and histopathological alterations as compared to Abeta (1-42) treated animals.	coq	15-20	tumor necrosis factor	Homo sapiens	342-351
26729958-13	2015	Administration of CoQ10 and CS resulted in a significant improvement of hepatic and renal functional parameters, and an improvement of both alpha-SMA and PCNA.	coq	18-23	actin gamma 2, smooth muscle	Rattus norvegicus	140-149
26729958-13	2015	Administration of CoQ10 and CS resulted in a significant improvement of hepatic and renal functional parameters, and an improvement of both alpha-SMA and PCNA.	coq	18-23	proliferating cell nuclear antigen	Rattus norvegicus	154-158
26185144-13	2015	The early mortality in our cohort suggests that COQ4 is an essential component of the multisubunit complex required for CoQ(10) biosynthesis.	coq	120-127	coenzyme Q4	Homo sapiens	48-52
27896114-2	2014	Ubiad1 protein was recently identified as Golgi prenyltransferase responsible for biosynthesis of vitamin K2 and CoQ10, a key protein in the mitochondrial electron transport chain.	coq	113-118	UbiA prenyltransferase domain containing 1	Homo sapiens	0-6
25801909-1	2015	INTRODUCTION: Recently, mutations in the COQ2 gene, encoding for an enzyme involved in coenzyme Q10 biosynthesis, have been suggested to confer susceptibility risk for multiple system atrophy (MSA).	coq	87-99	coenzyme Q2, polyprenyltransferase	Homo sapiens	41-45
25552930-10	2015	The protective effect of CoQ10 was associated with reduction in superoxide, normalization of mitochondrial membrane potential, improvement of mitochondrial respiration, inhibition of cyto-c release, suppression of caspase-9.	coq	25-30	cytochrome c, somatic	Homo sapiens	183-189
25552930-10	2015	The protective effect of CoQ10 was associated with reduction in superoxide, normalization of mitochondrial membrane potential, improvement of mitochondrial respiration, inhibition of cyto-c release, suppression of caspase-9.	coq	25-30	caspase 9	Homo sapiens	214-223
24986061-5	2015	Following consumption of Med + CoQ, hippurate excretion was positively correlated with CoQ and beta-carotene plasma levels and inversely related to Nrf2, thioredoxin, superoxide dismutase 1, and gp91(phox) subunit of NADPH oxidase gene expression.	coq	31-34	NFE2 like bZIP transcription factor 2	Homo sapiens	148-152
24986061-5	2015	Following consumption of Med + CoQ, hippurate excretion was positively correlated with CoQ and beta-carotene plasma levels and inversely related to Nrf2, thioredoxin, superoxide dismutase 1, and gp91(phox) subunit of NADPH oxidase gene expression.	coq	31-34	thioredoxin	Homo sapiens	154-165
24986061-5	2015	Following consumption of Med + CoQ, hippurate excretion was positively correlated with CoQ and beta-carotene plasma levels and inversely related to Nrf2, thioredoxin, superoxide dismutase 1, and gp91(phox) subunit of NADPH oxidase gene expression.	coq	31-34	superoxide dismutase 1	Homo sapiens	167-189
25789082-8	2015	These results indicated that CoQ10 could inhibit D-gal-induced MSC aging through the Akt/mTOR signaling.	coq	29-34	AKT serine/threonine kinase 1	Homo sapiens	85-88
25789082-8	2015	These results indicated that CoQ10 could inhibit D-gal-induced MSC aging through the Akt/mTOR signaling.	coq	29-34	mechanistic target of rapamycin kinase	Homo sapiens	89-93
25289702-1	2015	BACKGROUND: Multiple acyl-CoA dehydrogenase deficiency- (MADD-), also called glutaric aciduria type 2, associated leukodystrophy may be severe and progressive despite conventional treatment with protein- and fat-restricted diet, carnitine, riboflavin, and coenzyme Q10.	coq	256-268	MAP kinase activating death domain	Homo sapiens	57-61
24763291-5	2014	RESULTS: We identified a novel missense mutation (p.Asp208His; c.622G>C) in the coenzyme Q10 (CoQ10) biosynthesis monooxygenase 6 gene (COQ6) in schwannomatosis-affected members.	coq	80-92	putative N,N-dimethylaniline monooxygenase COQ6	Saccharomyces cerevisiae S288C	136-140
24763291-5	2014	RESULTS: We identified a novel missense mutation (p.Asp208His; c.622G>C) in the coenzyme Q10 (CoQ10) biosynthesis monooxygenase 6 gene (COQ6) in schwannomatosis-affected members.	coq	94-99	putative N,N-dimethylaniline monooxygenase COQ6	Saccharomyces cerevisiae S288C	136-140
25753843-7	2015	RESULTS: Our results showed that administration of CoQ10, amlodipine and their combination decreased colon tissue malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), prostaglandin E2 (PGE2), myeloperoxidase (MPO) and heat shock protein (HSP70) levels induced by intracolonic injection of acetic acid and restored many of the colon structure in histological examination.	coq	51-56	tumor necrosis factor	Rattus norvegicus	137-164
25753843-7	2015	RESULTS: Our results showed that administration of CoQ10, amlodipine and their combination decreased colon tissue malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), prostaglandin E2 (PGE2), myeloperoxidase (MPO) and heat shock protein (HSP70) levels induced by intracolonic injection of acetic acid and restored many of the colon structure in histological examination.	coq	51-56	tumor necrosis factor	Rattus norvegicus	166-175
25753843-7	2015	RESULTS: Our results showed that administration of CoQ10, amlodipine and their combination decreased colon tissue malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), prostaglandin E2 (PGE2), myeloperoxidase (MPO) and heat shock protein (HSP70) levels induced by intracolonic injection of acetic acid and restored many of the colon structure in histological examination.	coq	51-56	interleukin 1 beta	Rattus norvegicus	178-195
25753843-7	2015	RESULTS: Our results showed that administration of CoQ10, amlodipine and their combination decreased colon tissue malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), prostaglandin E2 (PGE2), myeloperoxidase (MPO) and heat shock protein (HSP70) levels induced by intracolonic injection of acetic acid and restored many of the colon structure in histological examination.	coq	51-56	interleukin 1 beta	Rattus norvegicus	197-205
25753843-7	2015	RESULTS: Our results showed that administration of CoQ10, amlodipine and their combination decreased colon tissue malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), prostaglandin E2 (PGE2), myeloperoxidase (MPO) and heat shock protein (HSP70) levels induced by intracolonic injection of acetic acid and restored many of the colon structure in histological examination.	coq	51-56	myeloperoxidase	Rattus norvegicus	233-248
25753843-7	2015	RESULTS: Our results showed that administration of CoQ10, amlodipine and their combination decreased colon tissue malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), prostaglandin E2 (PGE2), myeloperoxidase (MPO) and heat shock protein (HSP70) levels induced by intracolonic injection of acetic acid and restored many of the colon structure in histological examination.	coq	51-56	myeloperoxidase	Rattus norvegicus	250-253
25449974-4	2015	Cross-sectionally, exposure to CoQ10 was associated with lower SARA and higher UHDRS-IV scores in SCA1 and 3.	coq	31-36	ataxin 1	Homo sapiens	98-108
25449974-7	2015	CoQ10 is associated with better clinical outcome in SCA1 and 3.	coq	0-5	ataxin 1	Homo sapiens	52-62
25034304-0	2014	Inhibition of stress induced premature senescence in presenilin-1 mutated cells with water soluble Coenzyme Q10.	coq	99-111	presenilin 1	Homo sapiens	53-65
24659567-6	2014	CoQ10 treatments increased the activities of antioxidant enzymes (superoxide dismutase, GPx, catalase, glutathione S-transferase), protease inhibitors, biomarkers (aspartate aminotransferase, alkaline phosphatase, alanine aminotransferase), the total antioxidant potential level, and concentrations of uric acid and creatinine.	coq	0-5	Cat	Apis mellifera	93-101
24659567-6	2014	CoQ10 treatments increased the activities of antioxidant enzymes (superoxide dismutase, GPx, catalase, glutathione S-transferase), protease inhibitors, biomarkers (aspartate aminotransferase, alkaline phosphatase, alanine aminotransferase), the total antioxidant potential level, and concentrations of uric acid and creatinine.	coq	0-5	uncharacterized protein LOC552283	Apis mellifera	103-128
24632013-9	2014	In conclusion, CoQ10 protects against DOX-induced testicular toxicity in rats via ameliorating oxidative stress, reducing apoptosis and up-regulating testicular P-gp.	coq	15-20	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	161-165
24586567-6	2014	CoQ10 alone opposed the HFFD effect and increased the hepatic/muscular content/activity of tyrosine kinase (TK), phosphatidylinositol kinase (PI3K), and adiponectin receptors.	coq	0-5	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	153-164
23564352-2	2013	Analysis of TERE1 (aka UBIAD1) has shown it is a prenyltransferase enzyme in the natural bio-synthetic pathways for both vitamin K-2 and COQ10 production and exhibits multiple subcellular localizations including mitochondria, endoplasmic reticulum, and golgi.	coq	137-142	UbiA prenyltransferase domain containing 1	Homo sapiens	12-17
25672683-4	2014	COQ2 encodes an enzyme in the biosynthetic pathway of coenzyme Q10.	coq	54-66	coenzyme Q2, polyprenyltransferase	Homo sapiens	0-4
23532548-3	2013	Aim of this study is to verify the efficacy and safety of a nutraceutical complex containing Ginkgolide B/Coenzyme Q10/Riboflavin/Magnesium for prophylaxis in a sample of children affected by NF1 presenting migraine without aura.	coq	106-118	neurofibromin 1	Homo sapiens	192-195
23289958-2	2014	This randomised, placebo-controlled study examined the effect of CoQ10 on catalase, superoxide dismutase (SOD) and F2 -isoprostanes in seminal plasma in infertile men and their relation with CoQ10 concentration.	coq	65-70	catalase	Homo sapiens	74-82
24502382-7	2014	The recent identification of causal mutations and polymorphisms in COQ2, a gene encoding a biosynthetic enzyme for the production of the lipid-soluble electron carrier coenzyme Q10 (ubiquinone), puts membrane transporters as central to MSA pathogenesis, although how such transporters are involved in the early myelin degeneration observed in MSA remains unclear.	coq	168-180	coenzyme Q2, polyprenyltransferase	Homo sapiens	67-71
24270420-9	2013	Interestingly, a patient with SRNS with a homozygous ADCK4 frameshift mutation had partial remission following CoQ10 treatment.	coq	111-116	coenzyme Q8B	Homo sapiens	53-58
23532548-9	2013	In conclusion, the present study should be considered as the first report on the efficacy and safety of nutraceutical complex containing Ginkgolide B/Coenzyme Q10/Riboflavin/Magnesium for the prophylaxis of migraine in children affected by NF1.	coq	150-162	neurofibromin 1	Homo sapiens	240-243
23564352-2	2013	Analysis of TERE1 (aka UBIAD1) has shown it is a prenyltransferase enzyme in the natural bio-synthetic pathways for both vitamin K-2 and COQ10 production and exhibits multiple subcellular localizations including mitochondria, endoplasmic reticulum, and golgi.	coq	137-142	UbiA prenyltransferase domain containing 1	Homo sapiens	23-29
23977195-1	2013	UBIAD1 plays critical roles in physiology including vitamin K and CoQ10 biosynthesis as well as pathophysiology including dyslipimedia-induced SCD (Schnyder"s corneal dystrophy), Parkinson"s disease, cardiovascular disease and bladder carcinoma.	coq	66-71	UbiA prenyltransferase domain containing 1	Homo sapiens	0-6
23759948-2	2013	However, the profound effects of TERE1 relate to its prenyltransferase activity for synthesis of the bioactive quinones menaquinone and COQ10.	coq	136-141	UbiA prenyltransferase domain containing 1	Homo sapiens	33-38
22057896-6	2013	Med and Med + CoQ diets induced lower Nrf2, p22(phox), p47(phox), SOD1, SOD2 and TrxR gene expression and higher cytoplasmic Nrf2 and Keap-1 protein levels compared to the SFA diet.	coq	14-17	NFE2 like bZIP transcription factor 2	Homo sapiens	38-42
23430247-9	2013	The pretreatment of CoQ10 prevented EtOH-induced caspase-2 activation and mitochondria-mediated apoptosis.	coq	20-25	caspase 2	Homo sapiens	49-58
23509892-7	2013	Western blotting showed that CoQ10 treatment increased the expression levels of p85alpha PI3K, phosphorylated Akt (Ser473), phosphorylated glycogen synthase kinase-3beta (Ser9), and heat shock transcription factor, which are proteins related to the PI3K pathway in Abeta25-35 oligomers-treated NSCs.	coq	29-34	phosphoinositide-3-kinase regulatory subunit 2	Homo sapiens	80-93
23509892-7	2013	Western blotting showed that CoQ10 treatment increased the expression levels of p85alpha PI3K, phosphorylated Akt (Ser473), phosphorylated glycogen synthase kinase-3beta (Ser9), and heat shock transcription factor, which are proteins related to the PI3K pathway in Abeta25-35 oligomers-treated NSCs.	coq	29-34	AKT serine/threonine kinase 1	Homo sapiens	110-113
23509892-7	2013	Western blotting showed that CoQ10 treatment increased the expression levels of p85alpha PI3K, phosphorylated Akt (Ser473), phosphorylated glycogen synthase kinase-3beta (Ser9), and heat shock transcription factor, which are proteins related to the PI3K pathway in Abeta25-35 oligomers-treated NSCs.	coq	29-34	glycogen synthase kinase 3 beta	Homo sapiens	139-169
23199523-11	2013	There were also significant correlations between serum values of DHA, EPA, GLA and CoQ10 and serum PSA levels.	coq	83-88	kallikrein related peptidase 3	Homo sapiens	99-102
23199523-12	2013	The present study demonstrates that dietary supplements containing EPA, GLA or CoQ10 may significantly affect serum PSA levels.	coq	79-84	kallikrein related peptidase 3	Homo sapiens	116-119
22057896-6	2013	Med and Med + CoQ diets induced lower Nrf2, p22(phox), p47(phox), SOD1, SOD2 and TrxR gene expression and higher cytoplasmic Nrf2 and Keap-1 protein levels compared to the SFA diet.	coq	14-17	calcineurin like EF-hand protein 1	Homo sapiens	44-47
22057896-6	2013	Med and Med + CoQ diets induced lower Nrf2, p22(phox), p47(phox), SOD1, SOD2 and TrxR gene expression and higher cytoplasmic Nrf2 and Keap-1 protein levels compared to the SFA diet.	coq	14-17	pleckstrin	Homo sapiens	55-58
22057896-6	2013	Med and Med + CoQ diets induced lower Nrf2, p22(phox), p47(phox), SOD1, SOD2 and TrxR gene expression and higher cytoplasmic Nrf2 and Keap-1 protein levels compared to the SFA diet.	coq	14-17	superoxide dismutase 1	Homo sapiens	66-70
22057896-6	2013	Med and Med + CoQ diets induced lower Nrf2, p22(phox), p47(phox), SOD1, SOD2 and TrxR gene expression and higher cytoplasmic Nrf2 and Keap-1 protein levels compared to the SFA diet.	coq	14-17	superoxide dismutase 2	Homo sapiens	72-76
22057896-6	2013	Med and Med + CoQ diets induced lower Nrf2, p22(phox), p47(phox), SOD1, SOD2 and TrxR gene expression and higher cytoplasmic Nrf2 and Keap-1 protein levels compared to the SFA diet.	coq	14-17	NFE2 like bZIP transcription factor 2	Homo sapiens	125-129
22057896-6	2013	Med and Med + CoQ diets induced lower Nrf2, p22(phox), p47(phox), SOD1, SOD2 and TrxR gene expression and higher cytoplasmic Nrf2 and Keap-1 protein levels compared to the SFA diet.	coq	14-17	kelch like ECH associated protein 1	Homo sapiens	134-140
22057896-7	2013	Moreover, Med + CoQ diet produced lower postprandial Nrf2 gene expression and lower nuclear Nrf2 protein levels compared to the other diets and lower GPx1 gene expression than the SFA diet.	coq	16-19	NFE2 like bZIP transcription factor 2	Homo sapiens	53-57
22057896-7	2013	Moreover, Med + CoQ diet produced lower postprandial Nrf2 gene expression and lower nuclear Nrf2 protein levels compared to the other diets and lower GPx1 gene expression than the SFA diet.	coq	16-19	NFE2 like bZIP transcription factor 2	Homo sapiens	92-96
22057896-7	2013	Moreover, Med + CoQ diet produced lower postprandial Nrf2 gene expression and lower nuclear Nrf2 protein levels compared to the other diets and lower GPx1 gene expression than the SFA diet.	coq	16-19	glutathione peroxidase 1	Homo sapiens	150-154
22767283-4	2013	PABA is a competitive inhibitor of the CoQ(10) biosynthetic pathway enzyme, COQ2.	coq	39-46	coenzyme Q2, polyprenyltransferase	Homo sapiens	76-80
23150520-1	2013	Primary human CoQ(10) deficiencies are clinically heterogeneous diseases caused by mutations in PDSS2 and other genes required for CoQ(10) biosynthesis.	coq	14-21	decaprenyl diphosphate synthase subunit 2	Homo sapiens	96-101
23150520-1	2013	Primary human CoQ(10) deficiencies are clinically heterogeneous diseases caused by mutations in PDSS2 and other genes required for CoQ(10) biosynthesis.	coq	131-138	decaprenyl diphosphate synthase subunit 2	Homo sapiens	96-101
23150520-2	2013	Our in vitro studies of PDSS2 mutant fibroblasts, with &lt;20% CoQ(10) of control cells, revealed reduced activity of CoQ(10)-dependent complex II+III and ATP synthesis, without amplification of reactive oxygen species (ROS), markers of oxidative damage, or antioxidant defenses.	coq	63-66	prenyl (solanesyl) diphosphate synthase, subunit 2	Mus musculus	24-29
23150520-2	2013	Our in vitro studies of PDSS2 mutant fibroblasts, with &lt;20% CoQ(10) of control cells, revealed reduced activity of CoQ(10)-dependent complex II+III and ATP synthesis, without amplification of reactive oxygen species (ROS), markers of oxidative damage, or antioxidant defenses.	coq	118-121	prenyl (solanesyl) diphosphate synthase, subunit 2	Mus musculus	24-29
23150520-3	2013	In contrast, COQ2 and ADCK3 mutant fibroblasts, with 30-50% CoQ(10) of controls, showed milder bioenergetic defects but significantly increased ROS and oxidation of lipids and proteins.	coq	60-63	coenzyme Q2 4-hydroxybenzoate polyprenyltransferase	Mus musculus	13-17
23150520-3	2013	In contrast, COQ2 and ADCK3 mutant fibroblasts, with 30-50% CoQ(10) of controls, showed milder bioenergetic defects but significantly increased ROS and oxidation of lipids and proteins.	coq	60-63	coenzyme Q8A	Mus musculus	22-27
23267110-9	2013	These results suggest that reactive oxygen species and reduced PLCbeta3 expression may contribute to the sensory deficits in the late-stage diabetic db(-)/db(-) mouse, and that early long-term administration of the antioxidant CoQ10 may represent a promising therapeutic strategy for type 2 diabetes neuropathy.	coq	227-232	phospholipase C, beta 3	Mus musculus	63-71
23832331-2	2013	Dietary CoQ10 significantly reduced egg yolk cholesterol content and suppressed hepatic hydroxymethylglutaryl-CoA reductase (HMGR) activity.	coq	8-13	3-hydroxy-3-methylglutaryl-CoA reductase	Gallus gallus	88-123
23832331-2	2013	Dietary CoQ10 significantly reduced egg yolk cholesterol content and suppressed hepatic hydroxymethylglutaryl-CoA reductase (HMGR) activity.	coq	8-13	3-hydroxy-3-methylglutaryl-CoA reductase	Gallus gallus	125-129
21990004-7	2012	Data obtained also indicate that CoQ(10) prevents over-expression of TNF-alpha after exercise, together with an increase in sTNF-RII that limits the pro-inflammatory actions of TNF.	coq	33-36	tumor necrosis factor	Homo sapiens	69-78
23167655-4	2012	The effect of CoQ10 on evoked glutamate release was abolished by blocking the Cav2.2 (N-type) and Cav2.1 (P/Q-type) Ca2+ channels and mitogen-activated protein kinase kinase (MEK).	coq	14-19	calcium voltage-gated channel subunit alpha1 A	Rattus norvegicus	98-104
23167655-6	2012	Moreover, the inhibition of glutamate release by CoQ10 was strongly attenuated in mice without synapsin I.	coq	49-54	synapsin I	Mus musculus	95-105
21990004-7	2012	Data obtained also indicate that CoQ(10) prevents over-expression of TNF-alpha after exercise, together with an increase in sTNF-RII that limits the pro-inflammatory actions of TNF.	coq	33-36	tumor necrosis factor	Homo sapiens	69-72
22339577-4	2012	We demonstrated that CoQ(10)  treatment promoted proliferation of fibroblasts, increased type IV collagen expression and reduced UVR-induced matrix metalloproteinases-1 (MMP-1) level in embryonic and adult cells.	coq	21-28	matrix metallopeptidase 1	Homo sapiens	170-175
22231380-8	2012	The increasing number of molecular defects in enzymes of the CoQ(10) biosynthetic pathways (PDSS1, PDSS2, COQ2, COQ6, COQ9, CABC1/ADCK3) underlies the importance of these conditions.	coq	61-68	decaprenyl diphosphate synthase subunit 1	Homo sapiens	92-97
22231380-8	2012	The increasing number of molecular defects in enzymes of the CoQ(10) biosynthetic pathways (PDSS1, PDSS2, COQ2, COQ6, COQ9, CABC1/ADCK3) underlies the importance of these conditions.	coq	61-68	decaprenyl diphosphate synthase subunit 2	Homo sapiens	99-104
22231380-8	2012	The increasing number of molecular defects in enzymes of the CoQ(10) biosynthetic pathways (PDSS1, PDSS2, COQ2, COQ6, COQ9, CABC1/ADCK3) underlies the importance of these conditions.	coq	61-68	coenzyme Q2, polyprenyltransferase	Homo sapiens	106-110
22231380-8	2012	The increasing number of molecular defects in enzymes of the CoQ(10) biosynthetic pathways (PDSS1, PDSS2, COQ2, COQ6, COQ9, CABC1/ADCK3) underlies the importance of these conditions.	coq	61-68	coenzyme Q6, monooxygenase	Homo sapiens	112-116
22231380-8	2012	The increasing number of molecular defects in enzymes of the CoQ(10) biosynthetic pathways (PDSS1, PDSS2, COQ2, COQ6, COQ9, CABC1/ADCK3) underlies the importance of these conditions.	coq	61-68	coenzyme Q9	Homo sapiens	118-122
22231380-8	2012	The increasing number of molecular defects in enzymes of the CoQ(10) biosynthetic pathways (PDSS1, PDSS2, COQ2, COQ6, COQ9, CABC1/ADCK3) underlies the importance of these conditions.	coq	61-68	coenzyme Q8A	Homo sapiens	124-129
22231380-8	2012	The increasing number of molecular defects in enzymes of the CoQ(10) biosynthetic pathways (PDSS1, PDSS2, COQ2, COQ6, COQ9, CABC1/ADCK3) underlies the importance of these conditions.	coq	61-68	coenzyme Q8A	Homo sapiens	130-135
22339577-5	2012	In addition, CoQ(10)  treatment increased elastin gene expression in cultured fibroblasts and significantly decreased UVR-induced IL-1alpha production in HaCat cells.	coq	13-19	elastin	Homo sapiens	42-49
22339577-5	2012	In addition, CoQ(10)  treatment increased elastin gene expression in cultured fibroblasts and significantly decreased UVR-induced IL-1alpha production in HaCat cells.	coq	13-19	interleukin 1 alpha	Homo sapiens	130-139
22083459-7	2012	Furthermore, CoQ(10) treatment also reduced oxidative stress (as evident by reduced malondialdehyde, decreased ROS and increased Mn-SOD activity) in DDVP-treated rats" hippocampus region, along with enhanced activity of complexes I-III and complex IV.	coq	13-16	superoxide dismutase 2	Rattus norvegicus	129-135
21404051-2	2012	We explored whether the quality of dietary fat alters postprandial oxidative DNA damage and whether supplementation with CoQ improves antioxidant capacity by modifying the activation/stabilization of p53 in elderly subjects.	coq	121-124	tumor protein p53	Homo sapiens	200-203
21404051-8	2012	Moreover, Med+CoQ diet induced a postprandial decrease of cytoplasmatic p53, nuclear p-p53 (Ser20), and nuclear and cytoplasmatic monoubiquitinated p53 protein (p &lt; 0.05).	coq	14-17	tumor protein p53	Homo sapiens	72-75
21404051-8	2012	Moreover, Med+CoQ diet induced a postprandial decrease of cytoplasmatic p53, nuclear p-p53 (Ser20), and nuclear and cytoplasmatic monoubiquitinated p53 protein (p &lt; 0.05).	coq	14-17	tumor protein p53	Homo sapiens	87-90
21404051-8	2012	Moreover, Med+CoQ diet induced a postprandial decrease of cytoplasmatic p53, nuclear p-p53 (Ser20), and nuclear and cytoplasmatic monoubiquitinated p53 protein (p &lt; 0.05).	coq	14-17	tumor protein p53	Homo sapiens	87-90
22252298-10	2012	Together, CoQ10, selenite, and curcumin act as inhibitors of RANKL-induced NFATc1 which is a downstream event of NF-kappaB signal pathway through suppression of ROS generation, thereby suggesting their potential usefulness for the treatment of bone disease associated with excessive bone resorption.	coq	10-15	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	61-66
22368301-1	2012	BACKGROUND: COQ4 encodes a protein that organises the multienzyme complex for the synthesis of coenzyme Q(10) (CoQ(10)).	coq	111-114	coenzyme Q4	Homo sapiens	12-16
22368301-7	2012	Knockdown of COQ4 in HeLa cells also resulted in a reduction of CoQ(10.)	coq	64-67	coenzyme Q4	Homo sapiens	13-17
22252298-10	2012	Together, CoQ10, selenite, and curcumin act as inhibitors of RANKL-induced NFATc1 which is a downstream event of NF-kappaB signal pathway through suppression of ROS generation, thereby suggesting their potential usefulness for the treatment of bone disease associated with excessive bone resorption.	coq	10-15	nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 1	Mus musculus	75-81
21598008-3	2012	CoQ(10) significantly attenuated decrease in dopamine transporter as well as in synaptophysin and actin protein levels in DAergic synaptosomes from MPTP-treated mice.	coq	0-3	synaptophysin	Mus musculus	80-93
21812107-6	2011	Co Q10 rescued dephosphorylation of AMPK caused by oxLDL that in turn led to an activation of NADPH oxidase by PKC.	coq	0-6	2,4-dienoyl-CoA reductase 1	Homo sapiens	94-99
21170684-8	2011	Moreover, the Med+CoQ diet produced a lower postprandial decrease in total nitrite and a greater decrease in PC levels compared to the other two diets and lower SOD, CAT, and GPx activities than the SFA diet.In conclusion, Med diet reduces postprandial oxidative stress by reducing processes of cellular oxidation and increases the action of the antioxidant system in elderly persons and the administration of CoQ further improves this redox balance.	coq	18-21	superoxide dismutase 1	Homo sapiens	161-164
21849914-4	2011	We also observed an increased number of surviving CA3 neurons in 0.1 and 1 microM concentrations of CoQ10-treated groups using cresyl violet staining.	coq	100-105	carbonic anhydrase 3	Rattus norvegicus	50-53
22466841-0	2012	Coenzyme Q10 therapy in hereditary motor sensory neuropathy type VI with novel mitofusin 2 mutation.	coq	0-12	mitofusin 2	Homo sapiens	79-90
22466841-3	2012	A 37-year-old patient with HMSN VI with a novel mitofusin 2 mutation was treated with high dose of CoQ10 (200 mg/day) for eight months.	coq	99-104	mitofusin 2	Homo sapiens	48-59
22016358-4	2012	Med and Med + CoQ diets produced a lower fasting calreticulin, IL-1b, and JNK-1 gene expression; a lower postprandial p65, IKK-b, MMP-9, IL-1b, JNK-1, sXBP-1, and BiP/Grp78 gene expression; and a higher postprandial IkB-a gene expression compared with the SFA diet.	coq	14-17	calreticulin	Homo sapiens	49-61
22016358-4	2012	Med and Med + CoQ diets produced a lower fasting calreticulin, IL-1b, and JNK-1 gene expression; a lower postprandial p65, IKK-b, MMP-9, IL-1b, JNK-1, sXBP-1, and BiP/Grp78 gene expression; and a higher postprandial IkB-a gene expression compared with the SFA diet.	coq	14-17	interleukin 1 beta	Homo sapiens	63-68
22016358-4	2012	Med and Med + CoQ diets produced a lower fasting calreticulin, IL-1b, and JNK-1 gene expression; a lower postprandial p65, IKK-b, MMP-9, IL-1b, JNK-1, sXBP-1, and BiP/Grp78 gene expression; and a higher postprandial IkB-a gene expression compared with the SFA diet.	coq	14-17	mitogen-activated protein kinase 8	Homo sapiens	74-79
22016358-4	2012	Med and Med + CoQ diets produced a lower fasting calreticulin, IL-1b, and JNK-1 gene expression; a lower postprandial p65, IKK-b, MMP-9, IL-1b, JNK-1, sXBP-1, and BiP/Grp78 gene expression; and a higher postprandial IkB-a gene expression compared with the SFA diet.	coq	14-17	RELA proto-oncogene, NF-kB subunit	Homo sapiens	118-121
22016358-4	2012	Med and Med + CoQ diets produced a lower fasting calreticulin, IL-1b, and JNK-1 gene expression; a lower postprandial p65, IKK-b, MMP-9, IL-1b, JNK-1, sXBP-1, and BiP/Grp78 gene expression; and a higher postprandial IkB-a gene expression compared with the SFA diet.	coq	14-17	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	123-128
22016358-4	2012	Med and Med + CoQ diets produced a lower fasting calreticulin, IL-1b, and JNK-1 gene expression; a lower postprandial p65, IKK-b, MMP-9, IL-1b, JNK-1, sXBP-1, and BiP/Grp78 gene expression; and a higher postprandial IkB-a gene expression compared with the SFA diet.	coq	14-17	matrix metallopeptidase 9	Homo sapiens	130-135
22016358-4	2012	Med and Med + CoQ diets produced a lower fasting calreticulin, IL-1b, and JNK-1 gene expression; a lower postprandial p65, IKK-b, MMP-9, IL-1b, JNK-1, sXBP-1, and BiP/Grp78 gene expression; and a higher postprandial IkB-a gene expression compared with the SFA diet.	coq	14-17	interleukin 1 beta	Homo sapiens	137-142
22016358-4	2012	Med and Med + CoQ diets produced a lower fasting calreticulin, IL-1b, and JNK-1 gene expression; a lower postprandial p65, IKK-b, MMP-9, IL-1b, JNK-1, sXBP-1, and BiP/Grp78 gene expression; and a higher postprandial IkB-a gene expression compared with the SFA diet.	coq	14-17	mitogen-activated protein kinase 8	Homo sapiens	144-149
22016358-4	2012	Med and Med + CoQ diets produced a lower fasting calreticulin, IL-1b, and JNK-1 gene expression; a lower postprandial p65, IKK-b, MMP-9, IL-1b, JNK-1, sXBP-1, and BiP/Grp78 gene expression; and a higher postprandial IkB-a gene expression compared with the SFA diet.	coq	14-17	heat shock protein family A (Hsp70) member 5	Homo sapiens	163-166
22016358-4	2012	Med and Med + CoQ diets produced a lower fasting calreticulin, IL-1b, and JNK-1 gene expression; a lower postprandial p65, IKK-b, MMP-9, IL-1b, JNK-1, sXBP-1, and BiP/Grp78 gene expression; and a higher postprandial IkB-a gene expression compared with the SFA diet.	coq	14-17	heat shock protein family A (Hsp70) member 5	Homo sapiens	167-172
22016358-5	2012	Med + CoQ diet produced a lower postprandial decrease p65 and IKK-b gene expression compared with the other diets.	coq	6-9	RELA proto-oncogene, NF-kB subunit	Homo sapiens	54-57
22016358-5	2012	Med + CoQ diet produced a lower postprandial decrease p65 and IKK-b gene expression compared with the other diets.	coq	6-9	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	62-67
21556371-11	2011	In EtOH-exposed corneal fibroblasts, CoQ(10) pretreatment significantly reduced mitochondrial depolarization and ROS production at 30, 60, 90, and 120 min and inhibited the activation and expression of caspases 2 and 3 at 2 h after EtOH exposure.	coq	37-44	caspase 2	Homo sapiens	202-218
21483849-4	2011	Using recombinant NAD(P)H:quinone oxidoreductase (NQO) enzymes, we observed that contrary to CoQ10 short-chain quinones such as idebenone are good substrates for both NQO1 and NQO2.	coq	93-98	NAD(P)H quinone dehydrogenase 1	Homo sapiens	167-171
20889762-8	2010	Full rescue of the qless neural phenotype was achieved by dietary supplementation with CoQ4, CoQ9 or CoQ10, indicating that a side chain as short as four isoprenoid units can provide in vivo activity.	coq	101-106	qless	Drosophila melanogaster	19-24
22174665-11	2011	The protective effect of CoQ10 was associated with reduction in superoxide production, normalization of mitochondrial membrane potential and inhibition of caspase-9 and caspase-3 activation.	coq	25-30	caspase 9	Mus musculus	155-164
22174665-11	2011	The protective effect of CoQ10 was associated with reduction in superoxide production, normalization of mitochondrial membrane potential and inhibition of caspase-9 and caspase-3 activation.	coq	25-30	caspase 3	Mus musculus	169-178
22174665-12	2011	It is concluded that the neuroprotective effect of CoQ10 results from inhibiting oxidative stress and blocking caspase-3 dependent cell death pathway.	coq	51-56	caspase 3	Mus musculus	111-120
21799249-3	2011	Coenzyme Q10 (CoQ10), a component of the mitochondrial electron transport chain, is well characterized as a neuroprotective antioxidant in animal models and human trials of Huntington"s disease and Parkinson"s disease, and reduces plaque burden in AbetaPP/PS1 mice.	coq	0-12	presenilin 1	Homo sapiens	256-259
21799249-3	2011	Coenzyme Q10 (CoQ10), a component of the mitochondrial electron transport chain, is well characterized as a neuroprotective antioxidant in animal models and human trials of Huntington"s disease and Parkinson"s disease, and reduces plaque burden in AbetaPP/PS1 mice.	coq	14-19	presenilin 1	Homo sapiens	256-259
22715588-4	2011	CoQ10 significantly inhibited bFGF-induced angiogenesis in a mouse Matrigel plug and the sprouting of endothelial cells in rat aortic rings.	coq	0-5	fibroblast growth factor 2	Mus musculus	30-34
21086475-9	2010	In conclusion, the reduced form of CoQ(10) mediates distinct effects on cholesterol metabolism at the transcriptional and metabolite level in SAMP1 mice.	coq	35-42	transmembrane protein 201	Mus musculus	142-147