PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
34771486-3	2021	(2) Methods: We determined miR-33a expression levels following exposure of MCF-7 and MDA-MB-231 breast cancer cells to estrogen receptor (ER) activator (estradiol-17beta, E2) or anti-estrogens (ICI 182,780, Fulvestrant, FUL) at non-cytotoxic concentrations.	Estradiol	153-169	microRNA 33a	Homo sapiens	27-34
34771486-3	2021	(2) Methods: We determined miR-33a expression levels following exposure of MCF-7 and MDA-MB-231 breast cancer cells to estrogen receptor (ER) activator (estradiol-17beta, E2) or anti-estrogens (ICI 182,780, Fulvestrant, FUL) at non-cytotoxic concentrations.	Estradiol	171-173	microRNA 33a	Homo sapiens	27-34
34771486-6	2021	In contrast to the miR-33a inhibitor effect, miR-33a mimic co-transfection with E2 or FUL led to diminished AMP-activated protein kinase alpha (AMPKalpha) activity in MCF-7 cells.	Estradiol	80-82	microRNA 33a	Homo sapiens	45-52
34771486-8	2021	miR-33a inhibitor co-treatment suppressed E2-mediated AMPKalpha activity in MDA-MB-231 cells.	Estradiol	42-44	microRNA 33a	Homo sapiens	0-7
35534923-5	2022	METHODS: We used pH low-insertion peptide (pHLIP) constructs as vehicles to deliver microRNA-33-5p (miR-33) antisense oligonucleotides to atherosclerotic plaques.	Oligonucleotides	118-134	microRNA 33a	Homo sapiens	100-106
34513856-6	2021	Dietary cholesterol levels did not affect the microbiome and neither did alterations of plasma lipid levels through treatments of miR-33 antisense oligonucleotide (anti-miR-33), Niemann-Pick C1-Like 1 (NPC1L1) antisense oligonucleotide (ASO), and inducible degrader of LDLR (IDOL) ASO.	Oligonucleotides	147-162	microRNA 33a	Homo sapiens	130-136
33465419-11	2021	miR-18a-5p and miR-144-3p also had a significant direct correlation with miR-33a-5p, an important modulator of cholesterol homeostasis.	mir-18a-5p	0-10	microRNA 33a	Homo sapiens	73-80
35531134-2	2022	MiR-33a and miR-122 have a crucial role in cholesterol and lipid metabolism.	Cholesterol	43-54	microRNA 33a	Homo sapiens	0-7
35531134-8	2022	In addition, there was a significant negative correlation between miR-33a and miR-122 levels and PUFAs, total PUFAs/total SFAs ratio and omega 6 fatty acids.	Fatty Acids, Omega-6	137-156	microRNA 33a	Homo sapiens	66-73
35531134-9	2022	Conclusion and implications: Considering the roles of miR-33a and miR-122 in cholesterol and lipids metabolism, it may be concluded that the measurement of their expression may be useful as a potential additional biomarker for cardiometabolic derangement in T2DM patients.	Cholesterol	77-88	microRNA 33a	Homo sapiens	54-61
33898768-0	2021	miR-33a-5p in small extracellular vesicles as non-invasive biomarker for oxaliplatin sensitivity in human colorectal cancer cells.	Oxaliplatin	73-84	microRNA 33a	Homo sapiens	0-7
33898768-7	2021	In microarray and real-time RT-PCR analyses, the intracellular miR-33a-5p, miR-210-3p, and miR-224-5p expressions were lower in acquired and intrinsic L-OHP-resistant CRC cells than sensitive cells.	Oxaliplatin	151-156	microRNA 33a	Homo sapiens	63-70
33898768-11	2021	The amount of miR-33a-5p and miR-210-3p in sEVs secreted from acquired and intrinsic L-OHP-resistant cells tended to be small.	Oxaliplatin	85-90	microRNA 33a	Homo sapiens	14-21
33898768-13	2021	To the best of our knowledge, this is the first study demonstrating that miR-33a-5p and/or miR-210-3p in sEVs would be candidates for biomarkers of L-OHP sensitivity.	Oxaliplatin	148-153	microRNA 33a	Homo sapiens	73-80
33898768-14	2021	In particular, miR-33a-5p is a promising candidate because it would be directly involved in L-OHP sensitivity.	Oxaliplatin	92-97	microRNA 33a	Homo sapiens	15-22
33465419-11	2021	miR-18a-5p and miR-144-3p also had a significant direct correlation with miR-33a-5p, an important modulator of cholesterol homeostasis.	mir-144-3p	15-25	microRNA 33a	Homo sapiens	73-80
33465419-11	2021	miR-18a-5p and miR-144-3p also had a significant direct correlation with miR-33a-5p, an important modulator of cholesterol homeostasis.	Cholesterol	111-122	microRNA 33a	Homo sapiens	73-80
33538066-4	2022	Moreover, palbociclib treatment increased the levels of miR-33a in each cell line albeit a higher increase was evident in MiaPaCa-2 cells.	palbociclib	10-21	microRNA 33a	Homo sapiens	56-63
33721286-6	2021	Simvastatin also downregulated miR-33a expression.	Simvastatin	0-11	microRNA 33a	Homo sapiens	31-38
33744470-5	2021	In accord, miR-33 modulated ABCA1 expression and cholesterol efflux in human RPE cells.	Cholesterol	49-60	microRNA 33a	Homo sapiens	11-17
33744470-7	2021	These findings suggest that miR-33 targeting may decrease cholesterol deposition and ameliorate AMD initiation and progression.	Cholesterol	58-69	microRNA 33a	Homo sapiens	28-34
32782494-0	2020	Curcumin affects ox-LDL-induced IL-6, TNF-alpha, MCP-1 secretion and cholesterol efflux in THP-1 cells by suppressing the TLR4/NF-kappaB/miR33a signaling pathway.	Curcumin	0-8	microRNA 33a	Homo sapiens	137-143
33061613-10	2020	MiR-33a-5p expression was upregulated in GA-induced GC cells relative to GC cells.	gambogic acid	41-43	microRNA 33a	Homo sapiens	0-7
32782494-11	2020	Curcumin promoted cholesterol efflux by suppressing the TLR4/NF-kappaB/miR33a signaling pathway, and reduced the formation of foam cells and the secretion of inflammatory factors.	Curcumin	0-8	microRNA 33a	Homo sapiens	71-77
32782572-7	2020	miR-33a controls cellular cholesterol uptake and synthesis, which are both closely associated with carcinogenesis.	Cholesterol	26-37	microRNA 33a	Homo sapiens	0-7
32782494-11	2020	Curcumin promoted cholesterol efflux by suppressing the TLR4/NF-kappaB/miR33a signaling pathway, and reduced the formation of foam cells and the secretion of inflammatory factors.	Cholesterol	18-29	microRNA 33a	Homo sapiens	71-77
31673161-0	2020	Kidney miR-33 controls fatty acid oxidation.	Fatty Acids	23-33	microRNA 33a	Homo sapiens	7-13
32296037-4	2020	In this study, we observed that tacrolimus could induce triglyceride accumulation in hepatocytes by stimulating sterol response element-binding proteins (SREBPs) and miR-33a.	Tacrolimus	32-42	microRNA 33a	Homo sapiens	166-173
32296037-4	2020	In this study, we observed that tacrolimus could induce triglyceride accumulation in hepatocytes by stimulating sterol response element-binding proteins (SREBPs) and miR-33a.	Triglycerides	56-68	microRNA 33a	Homo sapiens	166-173
32296037-5	2020	Our in silico and experimental analyses identified miR-33a as a direct target of circFASN.	circfasn	81-89	microRNA 33a	Homo sapiens	51-58
32296037-6	2020	Tacrolimus could downregulate circFASN and result in elevated miR-33a in vivo and in vitro.	Tacrolimus	0-10	microRNA 33a	Homo sapiens	62-69
32296037-7	2020	Overexpression of circFASN or silencing of miR-33a decreased the promoting effects of tacrolimus on triglyceride accumulation.	Tacrolimus	86-96	microRNA 33a	Homo sapiens	43-50
32296037-7	2020	Overexpression of circFASN or silencing of miR-33a decreased the promoting effects of tacrolimus on triglyceride accumulation.	Triglycerides	100-112	microRNA 33a	Homo sapiens	43-50
32296037-9	2020	Our results showed that the circFASN/miR-33a regulatory system plays a distinct role in tacrolimus-induced disruption of lipid homeostasis.	Tacrolimus	88-98	microRNA 33a	Homo sapiens	37-44
32296037-10	2020	MiR-33a is likely a risk factor for tacrolimus-related dyslipidemia, providing a potential therapeutic target to combat tacrolimus-induced dyslipidemia after liver transplantation.	Tacrolimus	36-46	microRNA 33a	Homo sapiens	0-7
32296037-10	2020	MiR-33a is likely a risk factor for tacrolimus-related dyslipidemia, providing a potential therapeutic target to combat tacrolimus-induced dyslipidemia after liver transplantation.	Tacrolimus	120-130	microRNA 33a	Homo sapiens	0-7
32848718-0	2020	Delivery of microRNA-33 Antagomirs by Mesoporous Silica Nanoparticles to Ameliorate Lipid Metabolic Disorders.	mesoporous silica	38-55	microRNA 33a	Homo sapiens	12-23
32848718-3	2020	Recently, MicroRNA-33 (miR-33), a post-transcriptional regulator of genes involved in cholesterol efflux and fatty acid oxidation, has been considered as a good therapeutic target for these disorders.	Cholesterol	86-97	microRNA 33a	Homo sapiens	10-21
32848718-3	2020	Recently, MicroRNA-33 (miR-33), a post-transcriptional regulator of genes involved in cholesterol efflux and fatty acid oxidation, has been considered as a good therapeutic target for these disorders.	Cholesterol	86-97	microRNA 33a	Homo sapiens	23-29
32848718-3	2020	Recently, MicroRNA-33 (miR-33), a post-transcriptional regulator of genes involved in cholesterol efflux and fatty acid oxidation, has been considered as a good therapeutic target for these disorders.	Fatty Acids	109-119	microRNA 33a	Homo sapiens	10-21
32848718-3	2020	Recently, MicroRNA-33 (miR-33), a post-transcriptional regulator of genes involved in cholesterol efflux and fatty acid oxidation, has been considered as a good therapeutic target for these disorders.	Fatty Acids	109-119	microRNA 33a	Homo sapiens	23-29
32848718-5	2020	To counter this problem, in this study we used mesoporous silica nanoparticles (MSNs) as nanocarriers to deliver miR-33 antagomirs developing nanocomposites miR-MSNs.	mesoporous silica	47-64	microRNA 33a	Homo sapiens	113-119
32627938-5	2020	Moreover, circ-SPECC1 inhibited miR-33a expression by direct interaction, and miR-33a inhibitor partially reversed the effect of circ-SPECC1 knockdown on proliferation and apoptosis of H2 O2 -treated HCC cells.	Hydrogen Peroxide	185-190	microRNA 33a	Homo sapiens	32-39
32627938-5	2020	Moreover, circ-SPECC1 inhibited miR-33a expression by direct interaction, and miR-33a inhibitor partially reversed the effect of circ-SPECC1 knockdown on proliferation and apoptosis of H2 O2 -treated HCC cells.	Hydrogen Peroxide	185-190	microRNA 33a	Homo sapiens	78-85
32627938-7	2020	Meanwhile, autophagy inhibition by 3-methyladenine (3-MA) abrogated the effect of miR-33a mimics on proliferation and apoptosis of H2 O2 -treated HCC cells.	3-methyladenine	35-50	microRNA 33a	Homo sapiens	82-89
32627938-7	2020	Meanwhile, autophagy inhibition by 3-methyladenine (3-MA) abrogated the effect of miR-33a mimics on proliferation and apoptosis of H2 O2 -treated HCC cells.	3-methyladenine	52-56	microRNA 33a	Homo sapiens	82-89
32627938-7	2020	Meanwhile, autophagy inhibition by 3-methyladenine (3-MA) abrogated the effect of miR-33a mimics on proliferation and apoptosis of H2 O2 -treated HCC cells.	Hydrogen Peroxide	131-136	microRNA 33a	Homo sapiens	82-89
31257519-0	2019	Chidamide suppresses the glycolysis of triple negative breast cancer cells partially by targeting the miR-33a-5p-LDHA axis.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	0-9	microRNA 33a	Homo sapiens	102-109
31209892-4	2019	Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2), a mitochondrial enzyme involved in folic acid metabolism, interestingly was confirmed to be one of the target genes of miR-33a-5p in the present study.	Folic Acid	87-97	microRNA 33a	Homo sapiens	171-178
31017523-0	2019	Citrus peel flavonoids improve lipid metabolism by inhibiting miR-33 and miR-122 expression in HepG2 cells.	Flavonoids	12-22	microRNA 33a	Homo sapiens	62-68
31017523-5	2019	Flavonoid compounds from citrus peel suppressed miR-122 and miR-33 expression, which were induced by oleic acid.	Flavonoids	0-9	microRNA 33a	Homo sapiens	60-66
31017523-5	2019	Flavonoid compounds from citrus peel suppressed miR-122 and miR-33 expression, which were induced by oleic acid.	Oleic Acid	101-111	microRNA 33a	Homo sapiens	60-66
31669721-0	2019	Pseudoprotodioscin inhibits SREBPs and microRNA 33a/b levels and reduces the gene expression regarding the synthesis of cholesterol and triglycerides.	pseudo-protodioscin	0-18	microRNA 33a	Homo sapiens	39-53
31669721-15	2019	These studies demonstrated that PPD is a potential agent for cholesterol efflux, SREBPs and microRNA 33a/b inhibition, which related to the gene expression for the synthesis of cholesterol and triglycerides.	Cholesterol	177-188	microRNA 33a	Homo sapiens	92-106
31669721-15	2019	These studies demonstrated that PPD is a potential agent for cholesterol efflux, SREBPs and microRNA 33a/b inhibition, which related to the gene expression for the synthesis of cholesterol and triglycerides.	Triglycerides	193-206	microRNA 33a	Homo sapiens	92-106
31933767-0	2019	Tanshinone IIA reduces oxidized low-density lipoprotein-induced inflammatory responses by downregulating microRNA-33 in THP-1 macrophages.	tanshinone	0-14	microRNA 33a	Homo sapiens	105-116
31933767-10	2019	Tan inhibited pro-inflammatory cytokine secretion and miR-33 expression in ox-LDL-stimulated THP-1 macrophages.	tanshinone	0-3	microRNA 33a	Homo sapiens	54-60
31933767-12	2019	Moreover, miR-33 upregulation abrogated the inhibitory effect of Tan on pro-inflammatory cytokine secretion in ox-LDL-stimulated THP-1 macrophages.	tanshinone	65-68	microRNA 33a	Homo sapiens	10-16
31933767-13	2019	In conclusion, Tan inhibited ox-LDL-induced pro-inflammatory cytokine secretion by downregulating miR-33 in THP-1 macrophages, hinting that Tan might exert its atheroprotective effects by targeting miR-33 and reducing pro-inflammatory responses.	tanshinone	15-18	microRNA 33a	Homo sapiens	98-104
31933767-13	2019	In conclusion, Tan inhibited ox-LDL-induced pro-inflammatory cytokine secretion by downregulating miR-33 in THP-1 macrophages, hinting that Tan might exert its atheroprotective effects by targeting miR-33 and reducing pro-inflammatory responses.	tanshinone	15-18	microRNA 33a	Homo sapiens	198-204
31933767-13	2019	In conclusion, Tan inhibited ox-LDL-induced pro-inflammatory cytokine secretion by downregulating miR-33 in THP-1 macrophages, hinting that Tan might exert its atheroprotective effects by targeting miR-33 and reducing pro-inflammatory responses.	tanshinone	140-143	microRNA 33a	Homo sapiens	98-104
31933767-13	2019	In conclusion, Tan inhibited ox-LDL-induced pro-inflammatory cytokine secretion by downregulating miR-33 in THP-1 macrophages, hinting that Tan might exert its atheroprotective effects by targeting miR-33 and reducing pro-inflammatory responses.	tanshinone	140-143	microRNA 33a	Homo sapiens	198-204
31017523-7	2019	Citrus flavonoids likely regulate lipid metabolism by modulating the expression levels of miR-122 and miR-33.	Flavonoids	7-17	microRNA 33a	Homo sapiens	102-108
31257519-5	2019	Experiments investigating the underlying mechanism revealed that chidamide upregulated the expression of microRNA (miR)-33a-5p in TNBC cells via RT-qPCR.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	65-74	microRNA 33a	Homo sapiens	105-123
31257519-8	2019	Collectively, the results of the present study demonstrated that chidamide reprogramed glucose metabolism, partially by targeting the miR-33a-5p/LDHA pathway, in TNBC.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	65-74	microRNA 33a	Homo sapiens	134-141
30985366-4	2019	RECENT FINDINGS: The most widely studied of these miRNAs are miR-33a/b; however, we recently reported that miRNAs in the miR-183/96/182 cluster are also likely regulated by hepatic cholesterol content and mediate the observed glucose-lowering effects of the bile acid sequestrant colesevelam through the sterol-sensing pathway.	Cholesterol	181-192	microRNA 33a	Homo sapiens	61-68
30943047-17	2019	This study suggests that miR-33a inhibited EMT, invasion, and metastasis of GC through the Snail/Slug signaling pathway by modulating SNAI2 expression.NEW & NOTEWORTHY miR-33a targets and inhibits the expression of SNAI2, overexpression of SNAI2 activates the Snail/Slug signaling pathway, the Snail/Slug signaling pathway promotes GC cell proliferation, invasion, and metastasis, and overexpression of miR-33a inhibits cell proliferation, invasion, and metastasis.	Adenosine Monophosphate	156-159	microRNA 33a	Homo sapiens	25-32
30985366-4	2019	RECENT FINDINGS: The most widely studied of these miRNAs are miR-33a/b; however, we recently reported that miRNAs in the miR-183/96/182 cluster are also likely regulated by hepatic cholesterol content and mediate the observed glucose-lowering effects of the bile acid sequestrant colesevelam through the sterol-sensing pathway.	Glucose	226-233	microRNA 33a	Homo sapiens	61-68
30985366-4	2019	RECENT FINDINGS: The most widely studied of these miRNAs are miR-33a/b; however, we recently reported that miRNAs in the miR-183/96/182 cluster are also likely regulated by hepatic cholesterol content and mediate the observed glucose-lowering effects of the bile acid sequestrant colesevelam through the sterol-sensing pathway.	Bile Acids and Salts	258-267	microRNA 33a	Homo sapiens	61-68
30985366-4	2019	RECENT FINDINGS: The most widely studied of these miRNAs are miR-33a/b; however, we recently reported that miRNAs in the miR-183/96/182 cluster are also likely regulated by hepatic cholesterol content and mediate the observed glucose-lowering effects of the bile acid sequestrant colesevelam through the sterol-sensing pathway.	Sterols	186-192	microRNA 33a	Homo sapiens	61-68
30537863-2	2019	The miR-33 a/b has been shown to control the expression of genes involved in fatty acid biosynthesis, impaired metabolism and insulin resistance.	Fatty Acids	77-87	microRNA 33a	Homo sapiens	4-12
30022694-9	2019	There was a modest negative correlation between miR-33 and total cholesterol/high density lipoprotein ratio, triglycerides and very low density lipoprotein.	Triglycerides	109-122	microRNA 33a	Homo sapiens	48-54
30827510-4	2019	miR-33a and SREBP2 mRNA expression were inhibited by cholesterol, and when cells transfected with miR-33a mimics or inhibitor the effect of cholesterol appeared a significant difference than before.	Cholesterol	140-151	microRNA 33a	Homo sapiens	0-7
30827510-4	2019	miR-33a and SREBP2 mRNA expression were inhibited by cholesterol, and when cells transfected with miR-33a mimics or inhibitor the effect of cholesterol appeared a significant difference than before.	Cholesterol	140-151	microRNA 33a	Homo sapiens	98-105
30827510-6	2019	Thus, it inferred that cholesterol can regulate CRC development by miR-33a-PIM3 pathway.	Cholesterol	23-34	microRNA 33a	Homo sapiens	67-74
30777884-1	2019	Recent reports, including ours, have indicated that microRNA (miR)-33 located within the intron of sterol regulatory element binding protein (SREBP) 2 controls cholesterol homeostasis and can be a potential therapeutic target for the treatment of atherosclerosis.	Cholesterol	160-171	microRNA 33a	Homo sapiens	52-69
30827510-0	2019	Cholesterol regulates cell proliferation and apoptosis of colorectal cancer by modulating miR-33a-PIM3 pathway.	Cholesterol	0-11	microRNA 33a	Homo sapiens	90-97
30827510-2	2019	miR-33a was important in cholesterol metabolism and was abnormally expressed in many tumors, thus our study hypothesized that cholesterol effect on CRC by regulating miR-33a and its target gene PIM3, and verify it by series of assay.	Cholesterol	25-36	microRNA 33a	Homo sapiens	0-7
30827510-2	2019	miR-33a was important in cholesterol metabolism and was abnormally expressed in many tumors, thus our study hypothesized that cholesterol effect on CRC by regulating miR-33a and its target gene PIM3, and verify it by series of assay.	Cholesterol	126-137	microRNA 33a	Homo sapiens	0-7
30827510-2	2019	miR-33a was important in cholesterol metabolism and was abnormally expressed in many tumors, thus our study hypothesized that cholesterol effect on CRC by regulating miR-33a and its target gene PIM3, and verify it by series of assay.	Cholesterol	126-137	microRNA 33a	Homo sapiens	166-173
30827510-4	2019	miR-33a and SREBP2 mRNA expression were inhibited by cholesterol, and when cells transfected with miR-33a mimics or inhibitor the effect of cholesterol appeared a significant difference than before.	Cholesterol	53-64	microRNA 33a	Homo sapiens	0-7
29929012-4	2019	A number of miRNAs, including miR-33, miR-122 and miR-148a, have been demonstrated to play important role in controlling the risk of CVD through regulation of cholesterol homeostasis and lipoprotein metabolism.	Cholesterol	159-170	microRNA 33a	Homo sapiens	30-36
29183708-3	2018	Work from several groups has identified a number of miRNAs, including miR-33, miR-122 and miR-148a, that play a prominent role in controlling cholesterol homeostasis and lipoprotein metabolism.	Cholesterol	142-153	microRNA 33a	Homo sapiens	70-76
30389857-4	2018	We showed that miR-200c induces endothelial dysfunction, ROS production and a positive mechanism among miR-200c and miR-33a/b, two miRNAs involved in atherosclerosis progression.	Reactive Oxygen Species	57-60	microRNA 33a	Homo sapiens	116-123
30275686-5	2018	Results: The GO-CS-MPG-miR33a/miR199a nano drug-loading complex was successfully constructed and its medical effectiveness was verified.	go-cs	13-18	microRNA 33a	Homo sapiens	23-29
29551766-2	2018	Our published work implicates that TTF-1 positively regulates miR-33a which is known to repress ATP-binding cassette transporter 1 (ABCA1) and thus its cholesterol efflux activity.	Cholesterol	152-163	microRNA 33a	Homo sapiens	62-69
29601916-0	2018	B-RCA revealed circulating miR-33a/b associates with serum cholesterol in type 2 diabetes patients at high risk of ASCVD.	Cholesterol	59-70	microRNA 33a	Homo sapiens	27-34
29601916-7	2018	Pearson correlation coefficient was used to evaluate the correlation between circulating miR-33a/b and serum cholesterol.	Cholesterol	109-120	microRNA 33a	Homo sapiens	89-96
29601916-9	2018	Circulating miR-33a/b level is positively correlated with serum total cholesterol (TC) (r = 0.364, p = 0.048) and low-density lipoprotein cholesterol (LDL-C) (r = 0.383, p = 0.037) in T2D patients at high risk for developing ASCVD.	Cholesterol	70-81	microRNA 33a	Homo sapiens	12-19
29601916-9	2018	Circulating miR-33a/b level is positively correlated with serum total cholesterol (TC) (r = 0.364, p = 0.048) and low-density lipoprotein cholesterol (LDL-C) (r = 0.383, p = 0.037) in T2D patients at high risk for developing ASCVD.	Technetium	83-85	microRNA 33a	Homo sapiens	12-19
29601916-10	2018	CONCLUSIONS: Our B-RCA method provided an alternative strategy with specificity and high sensitivity for circulating miRNAs detection, and the results demonstrated that miR-33a/b might play an important role in cholesterol regulation.	Cholesterol	211-222	microRNA 33a	Homo sapiens	169-176
29653102-0	2018	Visceral adipose tissue-derived serine protease inhibitor accelerates cholesterol efflux by up-regulating ABCA1 expression via the NF-kappaB/miR-33a pathway in THP-1 macropahge-derived foam cells.	Cholesterol	70-81	microRNA 33a	Homo sapiens	141-148
29653102-4	2018	We found that vaspin decreased miR-33a levels, which in turn increased ABCA1 expression and cholesteorl efflux.	cholesteorl	92-103	microRNA 33a	Homo sapiens	31-38
29772548-4	2018	Accumulating studies have revealed that miRNAs such as miR-33, miR-27, miR-144, miR-758 and miR-20 are involved in the post-transcriptional control of ABCA1, ABCG1 and SCARB1 genes regulatory network of the reverse cholesterol transport (RCT).	Cholesterol	215-226	microRNA 33a	Homo sapiens	55-61
30466075-0	2018	miR-33a Mediates the Anti-Tumor Effect of Lovastatin in Osteosarcoma by Targeting CYR61.	Lovastatin	42-52	microRNA 33a	Homo sapiens	0-7
29243365-4	2018	C57BL/6 mice were treated with carbon tetrachloride for 4 weeks and concurrently given SREBP2-siRNA- or anti-miR-33a-bearing vitamin A-coupled liposomes.	Vitamin A	125-134	microRNA 33a	Homo sapiens	109-116
29243365-7	2018	Notably, in a mouse liver fibrosis model, reduction of FC accumulation, specifically in activated HSCs by suppression of SREBP2 or miR-33a expression using SREBP2-siRNA- or anti-miR-33a-bearing vitamin A-coupled liposomes, downregulated TLR4 signaling, increased Bambi expression, and consequently ameliorated liver fibrosis.	Fc(alpha) receptor	55-57	microRNA 33a	Homo sapiens	131-138
29243365-7	2018	Notably, in a mouse liver fibrosis model, reduction of FC accumulation, specifically in activated HSCs by suppression of SREBP2 or miR-33a expression using SREBP2-siRNA- or anti-miR-33a-bearing vitamin A-coupled liposomes, downregulated TLR4 signaling, increased Bambi expression, and consequently ameliorated liver fibrosis.	Fc(alpha) receptor	55-57	microRNA 33a	Homo sapiens	178-185
29243365-7	2018	Notably, in a mouse liver fibrosis model, reduction of FC accumulation, specifically in activated HSCs by suppression of SREBP2 or miR-33a expression using SREBP2-siRNA- or anti-miR-33a-bearing vitamin A-coupled liposomes, downregulated TLR4 signaling, increased Bambi expression, and consequently ameliorated liver fibrosis.	Vitamin A	194-203	microRNA 33a	Homo sapiens	178-185
29527188-0	2018	Polysaccharide IV from Lycium barbarum L. Improves Lipid Profiles of Gestational Diabetes Mellitus of Pregnancy by Upregulating ABCA1 and Downregulating Sterol Regulatory Element-Binding Transcription 1 via miR-33.	Polysaccharides	0-14	microRNA 33a	Homo sapiens	207-213
30466075-11	2018	Moreover, lovastatin increased the expression of SREBP-2 and miR-33a, which were then downregulated by SREBP-2 silencing.	Lovastatin	10-20	microRNA 33a	Homo sapiens	61-68
30466075-14	2018	SREBP-2 silencing or miR-33a inhibitor upregulated CYR61 expression and reversed the effects of lovastatin on cell invasion and EMT-related proteins.	Lovastatin	96-106	microRNA 33a	Homo sapiens	21-28
30466075-15	2018	CONCLUSION: Our findings suggest lovastatin suppresses osteosarcoma cell invasion through the SREBP-2/miR-33a/CYR61 pathway.	Lovastatin	33-43	microRNA 33a	Homo sapiens	102-109
29527188-13	2018	There was a strong positive association between miR-33 level and TG, or TC and or LDL-C, and a strong negative association between miR-33 level and HDL-C.	Triglycerides	65-67	microRNA 33a	Homo sapiens	48-54
29527188-13	2018	There was a strong positive association between miR-33 level and TG, or TC and or LDL-C, and a strong negative association between miR-33 level and HDL-C.	Technetium	72-74	microRNA 33a	Homo sapiens	48-54
29257274-7	2018	In addition, the results demonstrated that miR-33 impaired mitochondrial oxygen consumption rates, resulting in the accumulation of cellular reactive oxygen species, which stimulated NLRP3 expression, caspase-1 activity and IL-1beta secretion.	Oxygen	73-79	microRNA 33a	Homo sapiens	43-49
29257274-7	2018	In addition, the results demonstrated that miR-33 impaired mitochondrial oxygen consumption rates, resulting in the accumulation of cellular reactive oxygen species, which stimulated NLRP3 expression, caspase-1 activity and IL-1beta secretion.	Reactive Oxygen Species	141-164	microRNA 33a	Homo sapiens	43-49
28291769-9	2017	Oligonucleotide transfection showed that miR-33a-5p overexpression increased the cisplatin sensitivity of Hep3B/CDDP(v) and 97L/CDDP(v) drug-resistant cells and reduced their resistance.	Oligonucleotides	0-15	microRNA 33a	Homo sapiens	41-48
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	Imatinib Mesylate	16-24	microRNA 33a	Homo sapiens	228-234
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	ponatinib	29-38	microRNA 33a	Homo sapiens	228-234
29441904-8	2017	The increased CFB proliferation, and upregulation of Col-I, Col-III and alpha-SMA were all further enhanced by miR-33a mimic (P < 0.05 or P < 0.001), whereas reversed by miR-33a inhibitor (P < 0.05, P < 0.01 or P < 0.001).	alpha-sma	72-81	microRNA 33a	Homo sapiens	111-118
29180961-9	2017	Additionally, Rb1-reduced miR-33a and increased PEDF expression was prevented by pre-incubation with peroxisome proliferator-activated receptor-gamma (PPAR-gamma) antagonist (GW9662) or transfection with PPAR-gamma siRNA in HUVECs.	2-chloro-5-nitrobenzanilide	175-181	microRNA 33a	Homo sapiens	26-33
28811385-3	2017	miR-33a/b control cholesterol homoeostasis and recently miR-33b has been demonstrated to directly target the transcription factor zinc finger E-box-binding homeobox 1 (ZEB1).	Cholesterol	18-29	microRNA 33a	Homo sapiens	0-7
29137372-7	2017	Overexpression of miR-33a-5p enhanced the sensitivity of melanoma cells to X-radiation by MTT assay, while downregulation of miR-33a-5p had the opposite effects.	monooxyethylene trimethylolpropane tristearate	90-93	microRNA 33a	Homo sapiens	18-25
28291769-9	2017	Oligonucleotide transfection showed that miR-33a-5p overexpression increased the cisplatin sensitivity of Hep3B/CDDP(v) and 97L/CDDP(v) drug-resistant cells and reduced their resistance.	Cisplatin	81-90	microRNA 33a	Homo sapiens	41-48
28291769-10	2017	Additionally, inhibition of miR-33a-5p expression reduced cisplatin sensitivity in Hep3B and 97L and increased their drug resistance.	Cisplatin	58-67	microRNA 33a	Homo sapiens	28-35
28291769-11	2017	CONCLUSIONS This study confirmed that the most downregulated microRNA, miR-33a-5p, can mediate the cisplatin resistance of HCC cells, providing a new and feasible direction for research into combatting liver cancer chemotherapy resistance.	Cisplatin	99-108	microRNA 33a	Homo sapiens	71-78
27009502-4	2017	MiR-33a and MiR-33b play crucial roles in cholesterol and lipid metabolism, whereas miR-103 and miR-107 regulates hepatic insulin sensitivity.	Cholesterol	42-53	microRNA 33a	Homo sapiens	0-7
28994547-5	2017	microRNAs aggravate or reduce MIRI injury by down-regulating or up-regulating related genes expression, while miR-33, as a key regulator of cholesterol transport, regulates lipid metabolism through CROT, PGC-1alpha, AMPK and other genes located in the mitochondria.	Cholesterol	140-151	microRNA 33a	Homo sapiens	110-116
26223376-11	2016	Low levels of miR-335, miR-143 and miR-758, and high levels of miR-27, miR-378, miR-33 and miR-370 may have been responsible for elevated triglycerides and low-density lipoprotein (LDL-C) levels, and low level of high-density lipoprotein (HDL-C) in obese subjects.	Triglycerides	138-151	microRNA 33a	Homo sapiens	14-20
27664032-8	2017	The results suggest that enhanced expression of miR-33a might induce cholesterol accumulation and aggravate inflammation in vessel walls by suppressing the expression of ABCA1 in macrophages.	Cholesterol	69-80	microRNA 33a	Homo sapiens	48-55
27881008-0	2017	miR-33a expression sensitizes Lgr5+ HCC-CSCs to doxorubicin via ABCA1.	Doxorubicin	48-59	microRNA 33a	Homo sapiens	0-7
27881008-5	2017	We demonstrate that down-regulation of miR-33a expression directly contributes to chemo-resistance of Lgr5+ HCC-CSCs, and restoring miR-33a expression sensitizes them to doxorubicin via apoptosis by mainly using TUNEL assay, soft agar colony formation assay and xenograft assay.	Doxorubicin	170-181	microRNA 33a	Homo sapiens	132-139
27881008-7	2017	In conclusion, our work indicates that ectopic miR-33a expression sensitizes Lgr5+ HCC-CSCs to doxorubicin via direct targeting ABCA1, which sheds new light on understanding the mechanism of chemo-resistance in HCC-CSCs and contributes to development of potential therapeutics against HCC.	Doxorubicin	95-106	microRNA 33a	Homo sapiens	47-54
27923459-2	2016	In atherosclerosis, several miRNAs, such as miR-33a,b, miR-92a, miR-126 and others, have been identified that are relevant mediators of pathological processes, including regulation of cholesterol and lipid biosynthesis, lipoprotein metabolism and cholesterol efflux, but also immune responses, endothelial cell biology and vascular function.	Cholesterol	184-195	microRNA 33a	Homo sapiens	44-51
27923459-2	2016	In atherosclerosis, several miRNAs, such as miR-33a,b, miR-92a, miR-126 and others, have been identified that are relevant mediators of pathological processes, including regulation of cholesterol and lipid biosynthesis, lipoprotein metabolism and cholesterol efflux, but also immune responses, endothelial cell biology and vascular function.	Cholesterol	247-258	microRNA 33a	Homo sapiens	44-51
26945479-2	2016	miR-33 and miR-144 regulate adenosine triphosphate binding cassette transporter (ABCA1) and other target genes involved in cholesterol efflux, fatty acid oxidation and inflammation.	Cholesterol	123-134	microRNA 33a	Homo sapiens	0-6
26945479-2	2016	miR-33 and miR-144 regulate adenosine triphosphate binding cassette transporter (ABCA1) and other target genes involved in cholesterol efflux, fatty acid oxidation and inflammation.	Fatty Acids	143-153	microRNA 33a	Homo sapiens	0-6
27415822-3	2016	Treatment of human THP-1 cells with pitavastatin prevented the oxLDL-mediated suppression of miR-33a, -33b and -758 mRNA in these cells, an effect which was not uniquely attributable to induction of SREBP2.	pitavastatin	36-48	microRNA 33a	Homo sapiens	93-100
27116339-5	2016	Statistically significant (p<0.05) changes after exercise were found in 2 of the 8 miRNAs, namely, hsa-miR-33a (fold change, 7.66+-2.94; p=0.012), which regulates cholesterol homeostasis and fatty acid metabolism in the liver, and hsa-miR-378a (fold change 0.79+-0.11, p=0.048), which regulates energy homeostasis and affects lipogenesis and adipogenesis.	Cholesterol	166-177	microRNA 33a	Homo sapiens	102-113
27116339-5	2016	Statistically significant (p<0.05) changes after exercise were found in 2 of the 8 miRNAs, namely, hsa-miR-33a (fold change, 7.66+-2.94; p=0.012), which regulates cholesterol homeostasis and fatty acid metabolism in the liver, and hsa-miR-378a (fold change 0.79+-0.11, p=0.048), which regulates energy homeostasis and affects lipogenesis and adipogenesis.	Fatty Acids	194-204	microRNA 33a	Homo sapiens	102-113
27856248-9	2017	Conversely, inhibition of miR-33a by anti-miR-33a can rescue that using 4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and 5-ethynyl-2-deoxyuridine (EdU) assay.	4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-h-tetrazolium bromide	72-134	microRNA 33a	Homo sapiens	26-33
27856248-9	2017	Conversely, inhibition of miR-33a by anti-miR-33a can rescue that using 4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and 5-ethynyl-2-deoxyuridine (EdU) assay.	4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-h-tetrazolium bromide	72-134	microRNA 33a	Homo sapiens	42-49
27856248-9	2017	Conversely, inhibition of miR-33a by anti-miR-33a can rescue that using 4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and 5-ethynyl-2-deoxyuridine (EdU) assay.	monooxyethylene trimethylolpropane tristearate	136-139	microRNA 33a	Homo sapiens	26-33
27856248-9	2017	Conversely, inhibition of miR-33a by anti-miR-33a can rescue that using 4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and 5-ethynyl-2-deoxyuridine (EdU) assay.	monooxyethylene trimethylolpropane tristearate	136-139	microRNA 33a	Homo sapiens	42-49
27856248-9	2017	Conversely, inhibition of miR-33a by anti-miR-33a can rescue that using 4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and 5-ethynyl-2-deoxyuridine (EdU) assay.	5-ethynyl-2'-deoxyuridine	145-169	microRNA 33a	Homo sapiens	26-33
27856248-9	2017	Conversely, inhibition of miR-33a by anti-miR-33a can rescue that using 4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and 5-ethynyl-2-deoxyuridine (EdU) assay.	5-ethynyl-2'-deoxyuridine	145-169	microRNA 33a	Homo sapiens	42-49
27856248-9	2017	Conversely, inhibition of miR-33a by anti-miR-33a can rescue that using 4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and 5-ethynyl-2-deoxyuridine (EdU) assay.	5-ethynyl-2'-deoxyuridine	171-174	microRNA 33a	Homo sapiens	26-33
27856248-9	2017	Conversely, inhibition of miR-33a by anti-miR-33a can rescue that using 4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and 5-ethynyl-2-deoxyuridine (EdU) assay.	5-ethynyl-2'-deoxyuridine	171-174	microRNA 33a	Homo sapiens	42-49
26966281-4	2016	Statin therapy interferes with ATP-binding cassette transporter-mediated macrophage cholesterol efflux via miR33 and thus may diminish certain HDL functional properties.	Cholesterol	84-95	microRNA 33a	Homo sapiens	107-112
26941018-4	2016	APPROACH AND RESULTS: Here, we identify oxysterol-binding protein-like 6 (OSBPL6) as a novel target of 2 miRNA hubs regulating cholesterol homeostasis: miR-33 and miR-27b.	Cholesterol	127-138	microRNA 33a	Homo sapiens	152-158
26941018-11	2016	CONCLUSIONS: These studies identify ORP6 as a novel regulator of cholesterol trafficking that is part of the miR-33 and miR-27b target gene networks that contribute to the maintenance of cholesterol homeostasis.	Cholesterol	65-76	microRNA 33a	Homo sapiens	109-115
26941018-11	2016	CONCLUSIONS: These studies identify ORP6 as a novel regulator of cholesterol trafficking that is part of the miR-33 and miR-27b target gene networks that contribute to the maintenance of cholesterol homeostasis.	Cholesterol	187-198	microRNA 33a	Homo sapiens	109-115
27073545-1	2016	MicroRNA-33a (miR-33a) was previously identified as a lipid regulator that controls the cellular balance between cholesterol and fatty acid metabolism.	Cholesterol	113-124	microRNA 33a	Homo sapiens	0-12
27073545-1	2016	MicroRNA-33a (miR-33a) was previously identified as a lipid regulator that controls the cellular balance between cholesterol and fatty acid metabolism.	Cholesterol	113-124	microRNA 33a	Homo sapiens	14-21
27073545-1	2016	MicroRNA-33a (miR-33a) was previously identified as a lipid regulator that controls the cellular balance between cholesterol and fatty acid metabolism.	Fatty Acids	129-139	microRNA 33a	Homo sapiens	0-12
27073545-1	2016	MicroRNA-33a (miR-33a) was previously identified as a lipid regulator that controls the cellular balance between cholesterol and fatty acid metabolism.	Fatty Acids	129-139	microRNA 33a	Homo sapiens	14-21
27073545-6	2016	Furthermore, a bromodeoxyuridine incorporation assay and anaphase analysis revealed that miR-33a inhibits melanoma cell proliferation.	Bromodeoxyuridine	15-32	microRNA 33a	Homo sapiens	89-96
26938778-6	2016	Strikingly, we find miR-342-5p targets mevalonate-sterol biosynthesis using a multihit mechanism suppressing the pathway at different functional levels: transcriptionally via SREBF2, post-transcriptionally via miR-33, and enzymatically via IDI1 and SC4MOL.	Mevalonic Acid	39-49	microRNA 33a	Homo sapiens	210-216
26938778-6	2016	Strikingly, we find miR-342-5p targets mevalonate-sterol biosynthesis using a multihit mechanism suppressing the pathway at different functional levels: transcriptionally via SREBF2, post-transcriptionally via miR-33, and enzymatically via IDI1 and SC4MOL.	Sterols	50-56	microRNA 33a	Homo sapiens	210-216
26429200-9	2016	In ubiquinol supplementation group, alanine aminotransferase and alkaline phosphatase were significantly down-regulated after 12 weeks and changes in miR-15a, miR-21 and miR-33a were negatively correlated with alkaline phosphatase (p < 0.05).	ubiquinol	3-12	microRNA 33a	Homo sapiens	170-177
26602562-5	2015	METHODS: We investigated if atorvastatin can modulate the cholesterol related miR-33 family.	Atorvastatin	28-40	microRNA 33a	Homo sapiens	78-84
26830228-2	2016	The intronic microRNAs miR-33a and miR-33b, located within the genes encoding sterol regulatory element-binding protein 2 (SREBP-2) and SREBP-1, respectively, are transcribed in concert with their host genes and function alongside them to regulate cholesterol, fatty acid, and glucose metabolism.	Cholesterol	248-259	microRNA 33a	Homo sapiens	23-30
26830228-2	2016	The intronic microRNAs miR-33a and miR-33b, located within the genes encoding sterol regulatory element-binding protein 2 (SREBP-2) and SREBP-1, respectively, are transcribed in concert with their host genes and function alongside them to regulate cholesterol, fatty acid, and glucose metabolism.	Fatty Acids	261-271	microRNA 33a	Homo sapiens	23-30
26830228-2	2016	The intronic microRNAs miR-33a and miR-33b, located within the genes encoding sterol regulatory element-binding protein 2 (SREBP-2) and SREBP-1, respectively, are transcribed in concert with their host genes and function alongside them to regulate cholesterol, fatty acid, and glucose metabolism.	Glucose	277-284	microRNA 33a	Homo sapiens	23-30
26602562-5	2015	METHODS: We investigated if atorvastatin can modulate the cholesterol related miR-33 family.	Cholesterol	58-69	microRNA 33a	Homo sapiens	78-84
26229086-4	2015	miR-33a and miR-33b play a pivotal role in a variety of biological processes including cholesterol homoeostasis, HDL (high-density lipoprotein)-cholesterol formation, fatty acid oxidation and insulin signalling.	Cholesterol	87-98	microRNA 33a	Homo sapiens	0-7
26229086-4	2015	miR-33a and miR-33b play a pivotal role in a variety of biological processes including cholesterol homoeostasis, HDL (high-density lipoprotein)-cholesterol formation, fatty acid oxidation and insulin signalling.	Fatty Acids	167-177	microRNA 33a	Homo sapiens	0-7
26229086-10	2015	Although it is only explorative, the present study could be the first to point to the use of miR-33a and miR-33b as early biomarkers for cholesterol levels in childhood, once validated in independent larger cohorts.	Cholesterol	137-148	microRNA 33a	Homo sapiens	93-100
25810294-0	2015	SREBF2-embedded mir33 links the nuclear bile acid receptor FXR to cholesterol and lipoprotein metabolism.	Cholesterol	66-77	microRNA 33a	Homo sapiens	16-21
26113407-0	2015	miR-33a suppresses the nuclear translocation of beta-catenin to enhance gemcitabine sensitivity in human pancreatic cancer cells.	gemcitabine	72-83	microRNA 33a	Homo sapiens	0-7
26113407-4	2015	Moreover, gemcitabine (GEM) treatment enhanced beta-catenin expression by reducing miR-33a expression in a dose-dependent manner.	gemcitabine	10-21	microRNA 33a	Homo sapiens	83-90
26113407-4	2015	Moreover, gemcitabine (GEM) treatment enhanced beta-catenin expression by reducing miR-33a expression in a dose-dependent manner.	gemcitabine	23-26	microRNA 33a	Homo sapiens	83-90
26113407-5	2015	GEM-resistant MiaPaCa-2(res) cells with a low level of miR-33a expression and high level of beta-catenin expression adopted spindle-shaped morphologies, similar to their morphologies during the epithelial-to-mesenchymal transition (EMT), and their normal morphologies were restored by miR-33a overexpression.	gemcitabine	0-3	microRNA 33a	Homo sapiens	55-62
26113407-5	2015	GEM-resistant MiaPaCa-2(res) cells with a low level of miR-33a expression and high level of beta-catenin expression adopted spindle-shaped morphologies, similar to their morphologies during the epithelial-to-mesenchymal transition (EMT), and their normal morphologies were restored by miR-33a overexpression.	gemcitabine	0-3	microRNA 33a	Homo sapiens	285-292
26002865-3	2015	Bioinformatic pathway analysis predicts that miR-33 represses a cluster of genes controlling cellular energy metabolism that may be important in macrophage cholesterol efflux.	Cholesterol	156-167	microRNA 33a	Homo sapiens	45-51
26002865-4	2015	OBJECTIVE: We hypothesized that cellular energy status can influence cholesterol efflux from macrophages, and that miR-33 reduces cholesterol efflux via repression of mitochondrial energy metabolism pathways.	Cholesterol	130-141	microRNA 33a	Homo sapiens	115-121
26002865-6	2015	Inhibition of mitochondrial ATP synthase markedly reduces macrophage cholesterol efflux capacity, and anti-miR33 required fully functional mitochondria to enhance ABCA1-mediated cholesterol efflux.	Cholesterol	178-189	microRNA 33a	Homo sapiens	107-112
26002865-7	2015	Specifically, anti-miR33 derepressed the novel target genes PGC-1alpha, PDK4, and SLC25A25 and boosted mitochondrial respiration and production of ATP.	Adenosine Triphosphate	147-150	microRNA 33a	Homo sapiens	19-24
25971209-4	2015	Overexpression of miR-33a inhibited tumor cell proliferation and increased the chemosensitivity to gemcitabine both in vitro and in vivo.	gemcitabine	99-110	microRNA 33a	Homo sapiens	18-25
25971209-9	2015	Overall, these results indicate that miR-33a functions as a tumor suppressor that downregulates Pim-3 kinase expression to inhibit both pancreatic tumor growth and gemcitabine resistance via the AKT/beta-catenin pathway.	gemcitabine	164-175	microRNA 33a	Homo sapiens	37-44
25544258-5	2015	MTT assay results demonstrated that the overexpression of miR-33a significantly inhibited the proliferation of A549 cells, and similar results were obtained from the colony formation assay.	monooxyethylene trimethylolpropane tristearate	0-3	microRNA 33a	Homo sapiens	58-65
26352175-1	2015	Although microRNA-33 (miR-33) family members are known to be involved in the regulation and balancing of cholesterol metabolism, fatty acid oxidation and insulin signaling, their functions in carcinogenesis are controversial and the underlying mechanisms have remained elusive.	Cholesterol	105-116	microRNA 33a	Homo sapiens	22-28
26352175-1	2015	Although microRNA-33 (miR-33) family members are known to be involved in the regulation and balancing of cholesterol metabolism, fatty acid oxidation and insulin signaling, their functions in carcinogenesis are controversial and the underlying mechanisms have remained elusive.	Fatty Acids	129-139	microRNA 33a	Homo sapiens	22-28
26002865-10	2015	CONCLUSIONS: This study demonstrates that anti-miR33 therapy derepresses genes that enhance mitochondrial respiration and ATP production, which in conjunction with increased ABCA1 expression, works to promote macrophage cholesterol efflux and reduce atherosclerosis.	Adenosine Triphosphate	122-125	microRNA 33a	Homo sapiens	47-52
26002865-10	2015	CONCLUSIONS: This study demonstrates that anti-miR33 therapy derepresses genes that enhance mitochondrial respiration and ATP production, which in conjunction with increased ABCA1 expression, works to promote macrophage cholesterol efflux and reduce atherosclerosis.	Cholesterol	220-231	microRNA 33a	Homo sapiens	47-52
25544258-2	2015	miRNA-33a (miR-33a) is closely associated with cholesterol metabolism and is essential for cellular growth.	Cholesterol	47-58	microRNA 33a	Homo sapiens	0-9
25544258-2	2015	miRNA-33a (miR-33a) is closely associated with cholesterol metabolism and is essential for cellular growth.	Cholesterol	47-58	microRNA 33a	Homo sapiens	11-18
25880168-0	2015	MicroRNA-33a regulates cholesterol synthesis and cholesterol efflux-related genes in osteoarthritic chondrocytes.	Cholesterol	23-34	microRNA 33a	Homo sapiens	0-12
25155445-2	2015	Although microRNA-33a (miR-33a) is a novel modulator of lipid and cholesterol metabolism, the role of miR-33a in the hepatic fibrogenesis is still unknown.	Cholesterol	66-77	microRNA 33a	Homo sapiens	9-21
25155445-2	2015	Although microRNA-33a (miR-33a) is a novel modulator of lipid and cholesterol metabolism, the role of miR-33a in the hepatic fibrogenesis is still unknown.	Cholesterol	66-77	microRNA 33a	Homo sapiens	23-30
25880168-0	2015	MicroRNA-33a regulates cholesterol synthesis and cholesterol efflux-related genes in osteoarthritic chondrocytes.	Cholesterol	49-60	microRNA 33a	Homo sapiens	0-12
25880168-2	2015	On the basis of our previous findings on dysregulation of cholesterol homeostasis in OA, we were prompted to investigate whether microRNA-33a (miR-33a), one of the master regulators of cholesterol and fatty acid metabolism, plays a key role in OA pathogenesis.	Cholesterol	185-196	microRNA 33a	Homo sapiens	129-141
25880168-2	2015	On the basis of our previous findings on dysregulation of cholesterol homeostasis in OA, we were prompted to investigate whether microRNA-33a (miR-33a), one of the master regulators of cholesterol and fatty acid metabolism, plays a key role in OA pathogenesis.	Cholesterol	185-196	microRNA 33a	Homo sapiens	143-150
25880168-2	2015	On the basis of our previous findings on dysregulation of cholesterol homeostasis in OA, we were prompted to investigate whether microRNA-33a (miR-33a), one of the master regulators of cholesterol and fatty acid metabolism, plays a key role in OA pathogenesis.	Fatty Acids	201-211	microRNA 33a	Homo sapiens	129-141
25880168-2	2015	On the basis of our previous findings on dysregulation of cholesterol homeostasis in OA, we were prompted to investigate whether microRNA-33a (miR-33a), one of the master regulators of cholesterol and fatty acid metabolism, plays a key role in OA pathogenesis.	Fatty Acids	201-211	microRNA 33a	Homo sapiens	143-150
25880168-12	2015	CONCLUSIONS: Our findings suggest, for the first time to our knowledge, that miR-33a regulates cholesterol synthesis through the TGF-beta1/Akt/SREBP-2 pathway, as well as cholesterol efflux-related genes ABCA1 and ApoA1, in OA chondrocytes, pointing to its identification as a novel target for ameliorating the OA phenotype.	Cholesterol	95-106	microRNA 33a	Homo sapiens	77-84
24753547-1	2014	RATIONALE: Several reports suggest that antisense oligonucleotides against miR-33 might reduce cardiovascular risk in patients by accelerating the reverse cholesterol transport pathway.	Oligonucleotides	50-66	microRNA 33a	Homo sapiens	75-81
25744742-3	2015	There is emerging evidence linking miR-33a/b to lipid homoeostasis, targeting ABCA1,SREBF1, etc and it would appear that they have acted as "thrifty genes" during evolution to maintain cholesterol levels both at the cellular and whole body level.	Cholesterol	185-196	microRNA 33a	Homo sapiens	35-42
25749868-0	2015	Statin-induced decrease in ATP-binding cassette transporter A1 expression via microRNA33 induction may counteract cholesterol efflux to high-density lipoprotein.	Cholesterol	114-125	microRNA 33a	Homo sapiens	78-88
25749868-2	2015	In vitro, cholesterol depletion by statins is known to trigger a positive feedback on the cholesterol synthetic pathway via sterol regulatory element-binding protein (SREBP) transcription and changes in expression of SREBP regulated genes including microRNA33 (miR33) which is co-transcribed with SREBP and down-regulates ABCA1 and ABCG1 expression.	Cholesterol	10-21	microRNA 33a	Homo sapiens	249-259
25749868-2	2015	In vitro, cholesterol depletion by statins is known to trigger a positive feedback on the cholesterol synthetic pathway via sterol regulatory element-binding protein (SREBP) transcription and changes in expression of SREBP regulated genes including microRNA33 (miR33) which is co-transcribed with SREBP and down-regulates ABCA1 and ABCG1 expression.	Cholesterol	10-21	microRNA 33a	Homo sapiens	261-266
25749868-2	2015	In vitro, cholesterol depletion by statins is known to trigger a positive feedback on the cholesterol synthetic pathway via sterol regulatory element-binding protein (SREBP) transcription and changes in expression of SREBP regulated genes including microRNA33 (miR33) which is co-transcribed with SREBP and down-regulates ABCA1 and ABCG1 expression.	Cholesterol	90-101	microRNA 33a	Homo sapiens	249-259
25749868-2	2015	In vitro, cholesterol depletion by statins is known to trigger a positive feedback on the cholesterol synthetic pathway via sterol regulatory element-binding protein (SREBP) transcription and changes in expression of SREBP regulated genes including microRNA33 (miR33) which is co-transcribed with SREBP and down-regulates ABCA1 and ABCG1 expression.	Cholesterol	90-101	microRNA 33a	Homo sapiens	261-266
25749868-3	2015	METHODS: We investigated whether miR33 up-regulation, associated with SREBP increased transcription by statins, reduces macrophage ATP-binding cassette (ABC) transporter expression, thereby decreasing HDL-mediated cholesterol efflux at the tissue level.	Cholesterol	214-225	microRNA 33a	Homo sapiens	33-38
25749868-4	2015	RESULTS: In human macrophage THP-1 cells cholesterol-loaded with acetylated LDL, incubation with 1 muM atorvastatin increased miR33 by 33 % (P < 0.05), and decreased ABCA1 messenger RNA (mRNA) and ABCG1 mRNA by 47 % (P < 0.05) and 27 % (NS), respectively.	Atorvastatin	103-115	microRNA 33a	Homo sapiens	126-131
25202981-7	2014	PDE8A and UVRAG negatively regulated the cAMP/PKA and NOTCH pathways, respectively; therefore, miR-33a-dependent reduction of these proteins promoted growth and self-renewal of GICs by enhancing PKA and NOTCH activity.	Cyclic AMP	41-45	microRNA 33a	Homo sapiens	95-102
24753547-1	2014	RATIONALE: Several reports suggest that antisense oligonucleotides against miR-33 might reduce cardiovascular risk in patients by accelerating the reverse cholesterol transport pathway.	Cholesterol	155-166	microRNA 33a	Homo sapiens	75-81
24753547-2	2014	However, conflicting reports exist about the impact of anti-miR-33 therapy on the levels of very low-density lipoprotein-triglycerides (VLDL-TAG).	Triglycerides	121-134	microRNA 33a	Homo sapiens	60-66
24468065-0	2014	miR-33a is up-regulated in chemoresistant osteosarcoma and promotes osteosarcoma cell resistance to cisplatin by down-regulating TWIST.	Cisplatin	100-109	microRNA 33a	Homo sapiens	0-7
24468065-6	2014	In Saos-2 cells treated with cisplatin, inhibition of miR-33a by antagomir-33a markedly increased cell apoptosis, which was enhanced by overexpression of TWIST.	Cisplatin	29-38	microRNA 33a	Homo sapiens	54-61
24468065-8	2014	In MG-63 cells, overexpression of miR-33a significantly decreased cisplatin-induced cell apoptosis, which was enhanced by knockdown of TWIST.	Cisplatin	66-75	microRNA 33a	Homo sapiens	34-41
24468065-11	2014	Our in vitro data indicate that miR-33a promotes OS cell resistance to cisplatin by down-regulating TWIST; on the other hand, inhibition of miR-33a by antagomir-33a enhances cisplatin-induced apoptosis in OS cells by up-regulating TWIST expression.	Cisplatin	71-80	microRNA 33a	Homo sapiens	32-39
24468065-11	2014	Our in vitro data indicate that miR-33a promotes OS cell resistance to cisplatin by down-regulating TWIST; on the other hand, inhibition of miR-33a by antagomir-33a enhances cisplatin-induced apoptosis in OS cells by up-regulating TWIST expression.	Cisplatin	174-183	microRNA 33a	Homo sapiens	140-147
24100264-1	2014	MicroRNAs (miRNAs) attract more attention in the pathophysiology of liver fibrosis and miR-33a has been previously demonstrated as involved in the regulation of cholesterol and lipid metabolism.	Cholesterol	161-172	microRNA 33a	Homo sapiens	87-94
23716591-0	2013	MicroRNA 33 regulates glucose metabolism.	Glucose	22-29	microRNA 33a	Homo sapiens	0-11
24591767-9	2014	The changes of miR-33a and miR-33b were inversely related to the posttreatment LDL-C levels (r = -0.37, P = 0.019; r = -0.33, P = 0.035, resp.).	ldl-c	79-84	microRNA 33a	Homo sapiens	15-22
24591767-10	2014	CONCLUSION: In patients with low HDL-C levels, XZK therapy raised plasma levels of miR-33a and miR-33b, which may inhibit cellular cholesterol export and limit the HDL-raising effect of XZK.	Cholesterol	131-142	microRNA 33a	Homo sapiens	83-90
24165878-0	2014	Resveratrol and EGCG bind directly and distinctively to miR-33a and miR-122 and modulate divergently their levels in hepatic cells.	Resveratrol	0-11	microRNA 33a	Homo sapiens	56-63
24237343-6	2013	The data also suggest NRG1-alpha regulates genes (FBXO41) and miRNAs (miR-33) involved in cholesterol metabolism.	Cholesterol	90-101	microRNA 33a	Homo sapiens	70-76
24015284-0	2013	Aflatoxin B1 negatively regulates Wnt/beta-catenin signaling pathway through activating miR-33a.	Aflatoxin B1	0-12	microRNA 33a	Homo sapiens	88-95
24015284-3	2013	The level of miR-33a was up-regulated in hepatocellular carcinoma (HCC) cells treated with AFB1, while in the same cells causing the decrease in beta-catenin expression when treated at their IC50 values.	Aflatoxin B1	91-95	microRNA 33a	Homo sapiens	13-20
24015284-4	2013	miR-33a, specifically miR-33a-5p, was demonstrated to down-regulate the expression of beta-catenin, affect the beta-catenin pathway, and inhibit cell growth.	CHEMBL3740941	30-32	microRNA 33a	Homo sapiens	0-7
24015284-4	2013	miR-33a, specifically miR-33a-5p, was demonstrated to down-regulate the expression of beta-catenin, affect the beta-catenin pathway, and inhibit cell growth.	CHEMBL3740941	30-32	microRNA 33a	Homo sapiens	22-29
24165878-0	2014	Resveratrol and EGCG bind directly and distinctively to miR-33a and miR-122 and modulate divergently their levels in hepatic cells.	epigallocatechin gallate	16-20	microRNA 33a	Homo sapiens	56-63
24165878-7	2014	Therefore, the ability of resveratrol and epigallocatechin gallate to bind miR-33a and miR-122 was measured using (1)H NMR spectroscopy.	Resveratrol	26-37	microRNA 33a	Homo sapiens	75-82
24165878-7	2014	Therefore, the ability of resveratrol and epigallocatechin gallate to bind miR-33a and miR-122 was measured using (1)H NMR spectroscopy.	epigallocatechin gallate	42-66	microRNA 33a	Homo sapiens	75-82
24259050-8	2013	We show that pharmacological inhibition of the miR-33 family, key regulators of cholesterol/lipid homeostasis, by a subcutaneously delivered 8-mer LNA-modified antimiR in obese and insulin-resistant nonhuman primates results in derepression of miR-33 targets, such as ABCA1, increases circulating high-density lipoprotein cholesterol, and is well tolerated over 108 days of treatment.	Cholesterol	80-91	microRNA 33a	Homo sapiens	47-53
24259050-8	2013	We show that pharmacological inhibition of the miR-33 family, key regulators of cholesterol/lipid homeostasis, by a subcutaneously delivered 8-mer LNA-modified antimiR in obese and insulin-resistant nonhuman primates results in derepression of miR-33 targets, such as ABCA1, increases circulating high-density lipoprotein cholesterol, and is well tolerated over 108 days of treatment.	density lipoprotein cholesterol	302-333	microRNA 33a	Homo sapiens	47-53
23435093-6	2013	miRNA families miR-33, miR-758, miR-10b, miR-26 and miR-106b directly modulates cholesterol efflux by targeting the ATP-binding cassette transporter A1 (ABCA1).	106b	56-60	microRNA 33a	Homo sapiens	15-21
23435093-6	2013	miRNA families miR-33, miR-758, miR-10b, miR-26 and miR-106b directly modulates cholesterol efflux by targeting the ATP-binding cassette transporter A1 (ABCA1).	Cholesterol	80-91	microRNA 33a	Homo sapiens	15-21
23325474-4	2013	miR-33 controls cellular cholesterol export and fatty acid degradation, whereas its host genes stimulate cholesterol and fatty acid synthesis.	Cholesterol	25-36	microRNA 33a	Homo sapiens	0-6
23458685-9	2013	miR-33a overexpression also reduces the inhibitory activity of A549 on the production of OPG (osteoprotegerin), an osteoclastogenesis inhibitor.	a549	63-67	microRNA 33a	Homo sapiens	0-7
23562072-3	2013	(2013) now demonstrate that in aged macrophages decreased ABCA1 expression, regulated by liver X receptor and miR-33, impairs export of intracellular cholesterol, which promotes neovascular AMD.	Cholesterol	150-161	microRNA 33a	Homo sapiens	110-116
23547260-4	2013	Analogous to miR-33, miR-33* represses key enzymes involved in cholesterol efflux (ABCA1 and NPC1), fatty acid metabolism (CROT and CPT1a), and insulin signaling (IRS2).	Cholesterol	63-74	microRNA 33a	Homo sapiens	13-19
23547260-4	2013	Analogous to miR-33, miR-33* represses key enzymes involved in cholesterol efflux (ABCA1 and NPC1), fatty acid metabolism (CROT and CPT1a), and insulin signaling (IRS2).	Cholesterol	63-74	microRNA 33a	Homo sapiens	21-27
23547260-4	2013	Analogous to miR-33, miR-33* represses key enzymes involved in cholesterol efflux (ABCA1 and NPC1), fatty acid metabolism (CROT and CPT1a), and insulin signaling (IRS2).	Fatty Acids	100-110	microRNA 33a	Homo sapiens	13-19
23547260-4	2013	Analogous to miR-33, miR-33* represses key enzymes involved in cholesterol efflux (ABCA1 and NPC1), fatty acid metabolism (CROT and CPT1a), and insulin signaling (IRS2).	Fatty Acids	100-110	microRNA 33a	Homo sapiens	21-27
23547260-7	2013	Consistent with this, overexpression of miR-33* reduces fatty acid oxidation in human hepatic cells.	Fatty Acids	56-66	microRNA 33a	Homo sapiens	40-46
23325474-4	2013	miR-33 controls cellular cholesterol export and fatty acid degradation, whereas its host genes stimulate cholesterol and fatty acid synthesis.	Fatty Acids	48-58	microRNA 33a	Homo sapiens	0-6
23325474-4	2013	miR-33 controls cellular cholesterol export and fatty acid degradation, whereas its host genes stimulate cholesterol and fatty acid synthesis.	Cholesterol	105-116	microRNA 33a	Homo sapiens	0-6
23325474-4	2013	miR-33 controls cellular cholesterol export and fatty acid degradation, whereas its host genes stimulate cholesterol and fatty acid synthesis.	Fatty Acids	121-131	microRNA 33a	Homo sapiens	0-6
22274626-2	2012	Recently, microRNA-33a and b (miR-33a/b) were discovered as key regulators of metabolic programs including cholesterol and fatty acid homeostasis.	Cholesterol	107-118	microRNA 33a	Homo sapiens	10-28
22991041-7	2012	Finally, upregulation of macrophage cholesterol efflux pathways through agonism of liver X receptors or antagonism of miR-33 remains of substantial interest.	Cholesterol	36-47	microRNA 33a	Homo sapiens	118-124
22274626-4	2012	By repressing a variety of genes involved in cholesterol export and fatty acid oxidation, including  ABCA1,  CROT,  CPT1,  HADHB  and  PRKAA1, miR-33a/b act in concert with their host genes to boost cellular sterol levels.	Cholesterol	45-56	microRNA 33a	Homo sapiens	143-150
22274626-2	2012	Recently, microRNA-33a and b (miR-33a/b) were discovered as key regulators of metabolic programs including cholesterol and fatty acid homeostasis.	Cholesterol	107-118	microRNA 33a	Homo sapiens	30-37
22274626-4	2012	By repressing a variety of genes involved in cholesterol export and fatty acid oxidation, including  ABCA1,  CROT,  CPT1,  HADHB  and  PRKAA1, miR-33a/b act in concert with their host genes to boost cellular sterol levels.	Fatty Acids	68-78	microRNA 33a	Homo sapiens	143-150
22274626-2	2012	Recently, microRNA-33a and b (miR-33a/b) were discovered as key regulators of metabolic programs including cholesterol and fatty acid homeostasis.	Fatty Acids	123-133	microRNA 33a	Homo sapiens	10-28
22274626-4	2012	By repressing a variety of genes involved in cholesterol export and fatty acid oxidation, including  ABCA1,  CROT,  CPT1,  HADHB  and  PRKAA1, miR-33a/b act in concert with their host genes to boost cellular sterol levels.	Sterols	50-56	microRNA 33a	Homo sapiens	143-150
22274626-2	2012	Recently, microRNA-33a and b (miR-33a/b) were discovered as key regulators of metabolic programs including cholesterol and fatty acid homeostasis.	Fatty Acids	123-133	microRNA 33a	Homo sapiens	30-37
22436747-2	2012	For example, miR-33a and miR-33b have a crucial role in controlling cholesterol and lipid metabolism in concert with their host genes, the sterol-regulatory element-binding protein (SREBP) transcription factors.	Cholesterol	68-79	microRNA 33a	Homo sapiens	13-20
22391211-0	2012	MiR-33 connects cholesterol to the cell cycle.	Cholesterol	16-27	microRNA 33a	Homo sapiens	0-6
22012398-8	2011	Notably, miR-33 antagonism in this non-human primate model also increased the expression of miR-33 target genes involved in fatty acid oxidation (CROT, CPT1A, HADHB and PRKAA1) and reduced the expression of genes involved in fatty acid synthesis (SREBF1, FASN, ACLY and ACACA), resulting in a marked suppression of the plasma levels of very-low-density lipoprotein (VLDL)-associated triglycerides, a finding that has not previously been observed in mice.	Triglycerides	383-396	microRNA 33a	Homo sapiens	9-15
22315319-0	2012	miR-33a modulates ABCA1 expression, cholesterol accumulation, and insulin secretion in pancreatic islets.	Cholesterol	36-47	microRNA 33a	Homo sapiens	0-7
22315319-4	2012	We examined whether miR-33a regulates ABCA1 expression in pancreatic islets, thereby affecting cholesterol accumulation and insulin secretion.	Cholesterol	95-106	microRNA 33a	Homo sapiens	20-27
22315319-5	2012	Adenoviral miR-33a overexpression in human or mouse islets reduced ABCA1 expression, decreased glucose-stimulated insulin secretion, and increased cholesterol levels.	Glucose	95-102	microRNA 33a	Homo sapiens	11-18
22315319-5	2012	Adenoviral miR-33a overexpression in human or mouse islets reduced ABCA1 expression, decreased glucose-stimulated insulin secretion, and increased cholesterol levels.	Cholesterol	147-158	microRNA 33a	Homo sapiens	11-18
22315319-6	2012	The miR-33a-induced reduction in insulin secretion was rescued by cholesterol depletion by methyl-beta-cyclodextrin or mevastatin.	Cholesterol	66-77	microRNA 33a	Homo sapiens	4-11
22315319-6	2012	The miR-33a-induced reduction in insulin secretion was rescued by cholesterol depletion by methyl-beta-cyclodextrin or mevastatin.	methyl-beta-cyclodextrin	91-115	microRNA 33a	Homo sapiens	4-11
22315319-6	2012	The miR-33a-induced reduction in insulin secretion was rescued by cholesterol depletion by methyl-beta-cyclodextrin or mevastatin.	mevastatin	119-129	microRNA 33a	Homo sapiens	4-11
22333591-3	2012	Recent work from our group and others has shown that hsa-miR-33a and hsa-miR-33b, miRNAs located within intronic sequences of the Srebp genes, regulate cholesterol and fatty acid metabolism in concert with their host genes.	Cholesterol	152-163	microRNA 33a	Homo sapiens	53-64
22333591-3	2012	Recent work from our group and others has shown that hsa-miR-33a and hsa-miR-33b, miRNAs located within intronic sequences of the Srebp genes, regulate cholesterol and fatty acid metabolism in concert with their host genes.	Fatty Acids	168-178	microRNA 33a	Homo sapiens	53-64
22012398-0	2011	Inhibition of miR-33a/b in non-human primates raises plasma HDL and lowers VLDL triglycerides.	Triglycerides	80-93	microRNA 33a	Homo sapiens	14-21
22012398-4	2011	MicroRNA-33a and microRNA-33b (miR-33a/b) are intronic miRNAs whose encoding regions are embedded in the sterol-response-element-binding protein genes SREBF2 and SREBF1 (refs 3-5), respectively.	Sterols	105-111	microRNA 33a	Homo sapiens	31-38
22012398-7	2011	Here we show in African green monkeys that systemic delivery of an anti-miRNA oligonucleotide that targets both miR-33a and miR-33b increased hepatic expression of ABCA1 and induced a sustained increase in plasma HDL levels over 12 weeks.	Oligonucleotides	78-93	microRNA 33a	Homo sapiens	112-119
22012398-8	2011	Notably, miR-33 antagonism in this non-human primate model also increased the expression of miR-33 target genes involved in fatty acid oxidation (CROT, CPT1A, HADHB and PRKAA1) and reduced the expression of genes involved in fatty acid synthesis (SREBF1, FASN, ACLY and ACACA), resulting in a marked suppression of the plasma levels of very-low-density lipoprotein (VLDL)-associated triglycerides, a finding that has not previously been observed in mice.	Fatty Acids	124-134	microRNA 33a	Homo sapiens	9-15
22012398-8	2011	Notably, miR-33 antagonism in this non-human primate model also increased the expression of miR-33 target genes involved in fatty acid oxidation (CROT, CPT1A, HADHB and PRKAA1) and reduced the expression of genes involved in fatty acid synthesis (SREBF1, FASN, ACLY and ACACA), resulting in a marked suppression of the plasma levels of very-low-density lipoprotein (VLDL)-associated triglycerides, a finding that has not previously been observed in mice.	Fatty Acids	124-134	microRNA 33a	Homo sapiens	92-98
22012398-8	2011	Notably, miR-33 antagonism in this non-human primate model also increased the expression of miR-33 target genes involved in fatty acid oxidation (CROT, CPT1A, HADHB and PRKAA1) and reduced the expression of genes involved in fatty acid synthesis (SREBF1, FASN, ACLY and ACACA), resulting in a marked suppression of the plasma levels of very-low-density lipoprotein (VLDL)-associated triglycerides, a finding that has not previously been observed in mice.	Fatty Acids	225-235	microRNA 33a	Homo sapiens	9-15
22012398-9	2011	These data establish, in a model that is highly relevant to humans, that pharmacological inhibition of miR-33a and miR-33b is a promising therapeutic strategy to raise plasma HDL and lower VLDL triglyceride levels for the treatment of dyslipidaemias that increase cardiovascular disease risk.	Triglycerides	194-206	microRNA 33a	Homo sapiens	103-110
21548778-3	2011	Recent advances in the understanding of lipid metabolism have revealed that miRNAs, particularly miR-122 and miR-33, play major roles in regulating cholesterol and fatty acid homeostasis.	Cholesterol	148-159	microRNA 33a	Homo sapiens	109-115
21946517-3	2011	Of note is microRNA-33 (miR-33), an intronic microRNA (miRNA) located within the sterol regulatory element-binding protein (SREBP) genes, one of the master regulators of cholesterol and fatty acid metabolism.	Cholesterol	170-181	microRNA 33a	Homo sapiens	11-22
21946517-3	2011	Of note is microRNA-33 (miR-33), an intronic microRNA (miRNA) located within the sterol regulatory element-binding protein (SREBP) genes, one of the master regulators of cholesterol and fatty acid metabolism.	Cholesterol	170-181	microRNA 33a	Homo sapiens	24-30
21946517-3	2011	Of note is microRNA-33 (miR-33), an intronic microRNA (miRNA) located within the sterol regulatory element-binding protein (SREBP) genes, one of the master regulators of cholesterol and fatty acid metabolism.	Fatty Acids	186-196	microRNA 33a	Homo sapiens	11-22
21946517-3	2011	Of note is microRNA-33 (miR-33), an intronic microRNA (miRNA) located within the sterol regulatory element-binding protein (SREBP) genes, one of the master regulators of cholesterol and fatty acid metabolism.	Fatty Acids	186-196	microRNA 33a	Homo sapiens	24-30
21946517-4	2011	We have recently shown that miR-33 regulates cholesterol efflux and high-density lipoprotein (HDL) formation, as well as fatty acid oxidation and insulin signaling.	Cholesterol	45-56	microRNA 33a	Homo sapiens	28-34
21548778-3	2011	Recent advances in the understanding of lipid metabolism have revealed that miRNAs, particularly miR-122 and miR-33, play major roles in regulating cholesterol and fatty acid homeostasis.	Fatty Acids	164-174	microRNA 33a	Homo sapiens	109-115
21548778-5	2011	miR-33, an intronic miRNA located with the sterol response element-binding protein (SREBP)-2 gene, regulates cholesterol efflux, fatty acid beta oxidation, and high-density lipoprotein metabolism.	Cholesterol	109-120	microRNA 33a	Homo sapiens	0-6
21548778-5	2011	miR-33, an intronic miRNA located with the sterol response element-binding protein (SREBP)-2 gene, regulates cholesterol efflux, fatty acid beta oxidation, and high-density lipoprotein metabolism.	Fatty Acids	129-139	microRNA 33a	Homo sapiens	0-6
21576456-0	2011	miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling.	Fatty Acids	42-52	microRNA 33a	Homo sapiens	0-7
21576456-2	2011	Recent work from our group and others has shown that the intronic microRNAs hsa-miR-33a and hsa-miR-33b are located within the sterol regulatory element-binding protein-2 and -1 genes, respectively, and regulate cholesterol homeostasis in concert with their host genes.	Cholesterol	212-223	microRNA 33a	Homo sapiens	76-87
21576456-3	2011	Here, we show that miR-33a and -b also regulate genes involved in fatty acid metabolism and insulin signaling.	Fatty Acids	66-76	microRNA 33a	Homo sapiens	19-33
21576456-4	2011	miR-33a and -b target key enzymes involved in the regulation of fatty acid oxidation, including carnitine O-octaniltransferase, carnitine palmitoyltransferase 1A, hydroxyacyl-CoA-dehydrogenase, Sirtuin 6 (SIRT6), and AMP kinase subunit-alpha.	Fatty Acids	64-74	microRNA 33a	Homo sapiens	0-14
21576456-6	2011	Overexpression of miR-33a and -b reduces both fatty acid oxidation and insulin signaling in hepatic cell lines, whereas inhibition of endogenous miR-33a and -b increases these two metabolic pathways.	Fatty Acids	46-56	microRNA 33a	Homo sapiens	18-25
21576456-7	2011	Together, these data establish that miR-33a and -b regulate pathways controlling three of the risk factors of metabolic syndrome, namely levels of HDL, triglycerides, and insulin signaling, and suggest that inhibitors of miR-33a and -b may be useful in the treatment of this growing health concern.	Triglycerides	152-165	microRNA 33a	Homo sapiens	36-43
21576456-7	2011	Together, these data establish that miR-33a and -b regulate pathways controlling three of the risk factors of metabolic syndrome, namely levels of HDL, triglycerides, and insulin signaling, and suggest that inhibitors of miR-33a and -b may be useful in the treatment of this growing health concern.	Triglycerides	152-165	microRNA 33a	Homo sapiens	36-50
21285396-9	2011	This study uncovers a cholesterol-miR-33-RIP140 regulatory pathway that modulates the proinflammatory potential in macrophages in response to an alteration in the intracellular cholesterol status, and identifies RIP140 as a direct target of miR-33 that mediates simvastatin-triggered anti-inflammation.	Cholesterol	22-33	microRNA 33a	Homo sapiens	34-40
21285396-9	2011	This study uncovers a cholesterol-miR-33-RIP140 regulatory pathway that modulates the proinflammatory potential in macrophages in response to an alteration in the intracellular cholesterol status, and identifies RIP140 as a direct target of miR-33 that mediates simvastatin-triggered anti-inflammation.	Cholesterol	22-33	microRNA 33a	Homo sapiens	241-247
21285396-9	2011	This study uncovers a cholesterol-miR-33-RIP140 regulatory pathway that modulates the proinflammatory potential in macrophages in response to an alteration in the intracellular cholesterol status, and identifies RIP140 as a direct target of miR-33 that mediates simvastatin-triggered anti-inflammation.	Cholesterol	177-188	microRNA 33a	Homo sapiens	34-40
21285396-9	2011	This study uncovers a cholesterol-miR-33-RIP140 regulatory pathway that modulates the proinflammatory potential in macrophages in response to an alteration in the intracellular cholesterol status, and identifies RIP140 as a direct target of miR-33 that mediates simvastatin-triggered anti-inflammation.	Simvastatin	262-273	microRNA 33a	Homo sapiens	34-40
21178770-5	2011	Several reports have recently shown that miR-33 regulates cholesterol efflux and HDL biogenesis by downregulating the expression of the ABC transporters, ABCA1 and ABCG1.	Cholesterol	58-69	microRNA 33a	Homo sapiens	41-47
21178770-6	2011	In addition, miR-33 also inhibits the translation of several transcripts encoding proteins involved in fatty acid beta-oxidation including CPT1a, CROT, and HADHB, thereby reducing fatty acid degradation.	Fatty Acids	103-113	microRNA 33a	Homo sapiens	13-19
21178770-6	2011	In addition, miR-33 also inhibits the translation of several transcripts encoding proteins involved in fatty acid beta-oxidation including CPT1a, CROT, and HADHB, thereby reducing fatty acid degradation.	Fatty Acids	180-190	microRNA 33a	Homo sapiens	13-19
22156303-3	2011	Intriguingly, we recently discovered conserved microRNAs (miR-33a/b) embedded within intronic sequences of the human SREBF genes that act in a concerted manner with their host gene products to regulate cholesterol/lipid homeostasis.	Cholesterol	202-213	microRNA 33a	Homo sapiens	58-65
22156303-4	2011	Indeed, miR-33a/b control the levels of ATP-binding cassette (ABC) transporter ABCA1, a cholesterol efflux pump critical for high-density lipoprotein (HDL) synthesis and reverse cholesterol transport from peripheral tissues.	Cholesterol	88-99	microRNA 33a	Homo sapiens	8-15
20880716-3	2010	We and others have recently shown that miR-33 regulates cholesterol efflux and HDL biogenesis by downregulating the expression of the ABC transporters, ABCA1 and ABCG1.	Cholesterol	56-67	microRNA 33a	Homo sapiens	39-45
20880716-4	2010	In addition to miR-33, miR-122 and miR-370 have been shown to play important roles in regulating cholesterol and fatty acid metabolism.	Fatty Acids	113-123	microRNA 33a	Homo sapiens	15-21
20880716-4	2010	In addition to miR-33, miR-122 and miR-370 have been shown to play important roles in regulating cholesterol and fatty acid metabolism.	Cholesterol	97-108	microRNA 33a	Homo sapiens	15-21
20566875-5	2010	Our data show that LXR-dependent cholesterol efflux to both ApoAI and serum is ameliorated by miR-33 overexpression and, conversely, stimulated by miR-33 silencing.	Cholesterol	33-44	microRNA 33a	Homo sapiens	94-100
20732877-0	2010	Expression of miR-33 from an SREBP2 intron inhibits cholesterol export and fatty acid oxidation.	Cholesterol	52-63	microRNA 33a	Homo sapiens	14-20
20732877-0	2010	Expression of miR-33 from an SREBP2 intron inhibits cholesterol export and fatty acid oxidation.	Fatty Acids	75-85	microRNA 33a	Homo sapiens	14-20
20732877-3	2010	In this study, we provide evidence that the primary transcript of SREBP2 contains an intronic miRNA (miR-33) that reduces cellular cholesterol export via inhibition of translation of the cholesterol export pump ABCA1.	Cholesterol	131-142	microRNA 33a	Homo sapiens	101-107
20732877-3	2010	In this study, we provide evidence that the primary transcript of SREBP2 contains an intronic miRNA (miR-33) that reduces cellular cholesterol export via inhibition of translation of the cholesterol export pump ABCA1.	Cholesterol	187-198	microRNA 33a	Homo sapiens	101-107
20732877-4	2010	Notably, miR-33 also inhibits translation of several transcripts encoding proteins involved in fatty acid beta-oxidation including CPT1A, HADHB, and CROT, thereby reducing fatty acid degradation.	Fatty Acids	95-105	microRNA 33a	Homo sapiens	9-15
20732877-4	2010	Notably, miR-33 also inhibits translation of several transcripts encoding proteins involved in fatty acid beta-oxidation including CPT1A, HADHB, and CROT, thereby reducing fatty acid degradation.	Fatty Acids	172-182	microRNA 33a	Homo sapiens	9-15
20566875-5	2010	Our data show that LXR-dependent cholesterol efflux to both ApoAI and serum is ameliorated by miR-33 overexpression and, conversely, stimulated by miR-33 silencing.	Cholesterol	33-44	microRNA 33a	Homo sapiens	147-153
19386621-6	2009	The blockade of endogenous miR-338-3p or miR-451 via each microRNA-specific antisense oligonucleotides inhibited the translocalization of beta1 integrin to the basolateral membrane, whereas inhibition of miR-210 or miR-33a had no effect on it.	mir-338-3p	27-37	microRNA 33a	Homo sapiens	215-222
19386621-6	2009	The blockade of endogenous miR-338-3p or miR-451 via each microRNA-specific antisense oligonucleotides inhibited the translocalization of beta1 integrin to the basolateral membrane, whereas inhibition of miR-210 or miR-33a had no effect on it.	Oligonucleotides	86-102	microRNA 33a	Homo sapiens	215-222
20466882-3	2010	We show here that microRNAs (miR-33a/b) embedded within introns of the SREBP genes target the adenosine triphosphate-binding cassette transporter A1 (ABCA1), an important regulator of high-density lipoprotein (HDL) synthesis and reverse cholesterol transport, for posttranscriptional repression.	Cholesterol	237-248	microRNA 33a	Homo sapiens	29-36
20466882-5	2010	Our findings indicate that miR-33 acts in concert with the SREBP host genes to control cholesterol homeostasis and suggest that miR-33 may represent a therapeutic target for ameliorating cardiometabolic diseases.	Cholesterol	87-98	microRNA 33a	Homo sapiens	27-33
20466882-5	2010	Our findings indicate that miR-33 acts in concert with the SREBP host genes to control cholesterol homeostasis and suggest that miR-33 may represent a therapeutic target for ameliorating cardiometabolic diseases.	Cholesterol	87-98	microRNA 33a	Homo sapiens	128-134
20466885-3	2010	In mouse and human cells, miR-33 inhibits the expression of the adenosine triphosphate-binding cassette (ABC) transporter, ABCA1, thereby attenuating cholesterol efflux to apolipoprotein A1.	Cholesterol	150-161	microRNA 33a	Homo sapiens	26-32