PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33243020-4 2021 Results: Compared with telmisartan, ZnTelm displayed stronger binding to AT1R (binding studies on AT1R-transfected human embryonic kidney cells) and a greater reduction of reactive oxygen species and cytosolic calcium concentration induced by angiotensin II. Reactive Oxygen Species 172-195 angiotensinogen Homo sapiens 243-257 33624364-2 2021 Renin-angiotensin system (RAS) is elevated in septic subjects; accumulating studies show that angiotensin II (Ang II) stimulate the intrinsic apoptosis pathway by promoting reactive oxygen species (ROS) production. Reactive Oxygen Species 173-196 angiotensinogen Homo sapiens 94-108 33624364-2 2021 Renin-angiotensin system (RAS) is elevated in septic subjects; accumulating studies show that angiotensin II (Ang II) stimulate the intrinsic apoptosis pathway by promoting reactive oxygen species (ROS) production. Reactive Oxygen Species 173-196 angiotensinogen Homo sapiens 110-116 33624364-2 2021 Renin-angiotensin system (RAS) is elevated in septic subjects; accumulating studies show that angiotensin II (Ang II) stimulate the intrinsic apoptosis pathway by promoting reactive oxygen species (ROS) production. Reactive Oxygen Species 198-201 angiotensinogen Homo sapiens 94-108 33624364-2 2021 Renin-angiotensin system (RAS) is elevated in septic subjects; accumulating studies show that angiotensin II (Ang II) stimulate the intrinsic apoptosis pathway by promoting reactive oxygen species (ROS) production. Reactive Oxygen Species 198-201 angiotensinogen Homo sapiens 110-116 33792231-4 2021 In particular, angiotensin II (Ang II) through the generation of reactive oxygen species, induces a low grade of inflammation, which impairs the insulin signal transduction. Reactive Oxygen Species 65-88 angiotensinogen Homo sapiens 15-29 33792231-4 2021 In particular, angiotensin II (Ang II) through the generation of reactive oxygen species, induces a low grade of inflammation, which impairs the insulin signal transduction. Reactive Oxygen Species 65-88 angiotensinogen Homo sapiens 31-37 32372557-0 2020 Calcitonin gene-related peptide inhibits angiotensin II-induced NADPH oxidase-dependent ROS via the Src/STAT3 signalling pathway. Reactive Oxygen Species 88-91 angiotensinogen Homo sapiens 41-55 33162896-0 2020 Angiotensin II Decreases Endothelial Nitric Oxide Synthase Phosphorylation via AT1R Nox/ROS/PP2A Pathway. Reactive Oxygen Species 88-91 angiotensinogen Homo sapiens 0-14 32763515-0 2020 Nicotinamide nucleotide transhydrogenase (NNT) regulates mitochondrial ROS and endothelial dysfunction in response to angiotensin II. Reactive Oxygen Species 71-74 angiotensinogen Homo sapiens 118-132 32372557-4 2020 CGRP significantly suppressed the level of reactive oxygen species (ROS) generated by NADPH oxidase in Ang II-induced VSMCs. Reactive Oxygen Species 43-66 angiotensinogen Homo sapiens 103-109 32372557-4 2020 CGRP significantly suppressed the level of reactive oxygen species (ROS) generated by NADPH oxidase in Ang II-induced VSMCs. Reactive Oxygen Species 68-71 angiotensinogen Homo sapiens 103-109 32372557-8 2020 Additionally, both in vitro and in vivo analyses show that CGRP treatment inhibited Ang II-induced VSMC proliferation and hypertrophy, accompanied by a reduction in ROS generation. Reactive Oxygen Species 165-168 angiotensinogen Homo sapiens 84-90 32119711-6 2020 The TUNEL-positive cells as well as activated caspase 3, NADPH oxidase 4 protein (Nox4) and ROS levels were dramatically increased in Ang II-treated podocytes, which was prevented by secinH3, an Arf6 activity inhibitor. Reactive Oxygen Species 92-95 angiotensinogen Homo sapiens 134-140 32119711-8 2020 Ang II-induced elevation of Nox4 and ROS was prevented by Arf6 knockdown. Reactive Oxygen Species 37-40 angiotensinogen Homo sapiens 0-6 32119711-12 2020 Our data demonstrated that Ang II promotes ROS production and podocytes injury through activation of Arf6-Erk1/2-Nox4 signaling. Reactive Oxygen Species 43-46 angiotensinogen Homo sapiens 27-33 31668374-0 2020 Calcitonin gene-related peptide attenuates angiotensin II-induced ROS-dependent apoptosis in vascular smooth muscle cells by inhibiting the CaMKII/CREB signalling pathway. Reactive Oxygen Species 66-69 angiotensinogen Homo sapiens 43-57 31991780-6 2020 Moreover, the angiotensin II (AngII)-induced reactive oxygen species (ROS) production was blunted in the presence of nHDL, whereas it was preserved when the cells were preincubated with S1P receptor antagonists, suggesting that S1P accounts for the vascular protective function of nHDL at the feto-placental unit. Reactive Oxygen Species 45-68 angiotensinogen Homo sapiens 14-28 31991780-6 2020 Moreover, the angiotensin II (AngII)-induced reactive oxygen species (ROS) production was blunted in the presence of nHDL, whereas it was preserved when the cells were preincubated with S1P receptor antagonists, suggesting that S1P accounts for the vascular protective function of nHDL at the feto-placental unit. Reactive Oxygen Species 45-68 angiotensinogen Homo sapiens 30-35 31991780-6 2020 Moreover, the angiotensin II (AngII)-induced reactive oxygen species (ROS) production was blunted in the presence of nHDL, whereas it was preserved when the cells were preincubated with S1P receptor antagonists, suggesting that S1P accounts for the vascular protective function of nHDL at the feto-placental unit. Reactive Oxygen Species 70-73 angiotensinogen Homo sapiens 14-28 31991780-6 2020 Moreover, the angiotensin II (AngII)-induced reactive oxygen species (ROS) production was blunted in the presence of nHDL, whereas it was preserved when the cells were preincubated with S1P receptor antagonists, suggesting that S1P accounts for the vascular protective function of nHDL at the feto-placental unit. Reactive Oxygen Species 70-73 angiotensinogen Homo sapiens 30-35 30707954-5 2019 Angiotensin II, the active peptide of the renin-angiotensin-system (RAS), is a significant stimulus for ROS generation within the vasculature. Reactive Oxygen Species 104-107 angiotensinogen Homo sapiens 0-14 31265839-9 2019 Moreover, knockdown of Nrf2 significantly blocked the SIRT6-mediated protection effect against Ang II-induced apoptosis and reactive oxygen species generation. Reactive Oxygen Species 124-147 angiotensinogen Homo sapiens 95-101 30844388-7 2019 Since these metabolic pathways are related to calcium balance and oxidative stress, we further verified that angiotensin-(1-7) suppressed the abnormal extracellular calcium influx and excessive accumulation of intracellular reactive oxygen species (ROS) in angiotensin II-stimulated cardiac fibroblasts. Reactive Oxygen Species 224-247 angiotensinogen Homo sapiens 257-271 30844388-7 2019 Since these metabolic pathways are related to calcium balance and oxidative stress, we further verified that angiotensin-(1-7) suppressed the abnormal extracellular calcium influx and excessive accumulation of intracellular reactive oxygen species (ROS) in angiotensin II-stimulated cardiac fibroblasts. Reactive Oxygen Species 249-252 angiotensinogen Homo sapiens 257-271 31318113-0 2019 Protocatechuic acid attenuates angiotensin II-induced cardiac fibrosis in cardiac fibroblasts through inhibiting the NOX4/ROS/p38 signaling pathway. Reactive Oxygen Species 122-125 angiotensinogen Homo sapiens 31-45 31318113-9 2019 These findings showed that PCA treatment prevented the Ang II-induced cardiac fibrosis by inhibiting the NOX4/ROS/p38 signaling pathway in vitro, suggesting that PCA might be a therapeutic agent for MI. Reactive Oxygen Species 110-113 angiotensinogen Homo sapiens 55-61 31145308-7 2019 RESULTS: Compared with the control group, the cell viability and the rate of S phase cells in Ang II group significantly decreased (P < .05) while the apoptosis percentage and the levels of ROS, IL-8, TNF-alpha, TGF-beta1, and LDH in Ang II group significantly increased (P < .05). Reactive Oxygen Species 193-196 angiotensinogen Homo sapiens 94-100 30127931-7 2018 Therefore, it was demonstrated that puerarin on suppressed the cell growth of angiotensin II-induced aortic aneurysm formation by affecting the rate of apoptosis, the generation of ROS, MMP-2, AP-1 and p-Jun protein expression and NADPH oxidase. Reactive Oxygen Species 181-184 angiotensinogen Homo sapiens 78-92 29486589-8 2019 In vitro, AngII promoted intercellular ROS, hydrogen peroxide, and NADPH oxidase 4 (NOX4) protein levels and reduced the glutathione concentration, thereby leading to NLRP3 inflammasome activation and consequent collagen synthesis. Reactive Oxygen Species 39-42 angiotensinogen Homo sapiens 10-15 29486589-12 2019 Innovation and Conclusion: Autophagy attenuates pulmonary fibrosis by regulating NLRP3 inflammasome activation induced by AngII-mediated ROS via redox balance modulation. Reactive Oxygen Species 137-140 angiotensinogen Homo sapiens 122-127 30620754-0 2019 Ligand-activated PPARdelta inhibits angiotensin II-stimulated hypertrophy of vascular smooth muscle cells by targeting ROS. Reactive Oxygen Species 119-122 angiotensinogen Homo sapiens 36-50 30620754-3 2019 GW501516-activated PPARdelta also suppressed Ang II-induced generation of reactive oxygen species (ROS) in VSMCs. Reactive Oxygen Species 74-97 angiotensinogen Homo sapiens 45-51 30620754-3 2019 GW501516-activated PPARdelta also suppressed Ang II-induced generation of reactive oxygen species (ROS) in VSMCs. Reactive Oxygen Species 99-102 angiotensinogen Homo sapiens 45-51 29977005-10 2018 Our results demonstrate that ClC-3 acts as a positive regulator of Ang II-induced NADPH oxidase activation and ROS production in endothelial cells, possibly via promoting both Nox2/p22phox expression and p38 MAPK-dependent p47phox/p67phox membrane translocation, then increasing Nox2 NADPH oxidase complex formation. Reactive Oxygen Species 111-114 angiotensinogen Homo sapiens 67-73 31038541-1 2019 Besides stimulating vasoconstriction, Angiotensin II is also well known in inducing reactive oxygen species and promoting inflammatory phenotype switch via its type 1 receptor. Reactive Oxygen Species 84-107 angiotensinogen Homo sapiens 38-52 30338935-0 2019 Cardiac-specific Mst1 deficiency inhibits ROS-mediated JNK signalling to alleviate Ang II-induced cardiomyocyte apoptosis. Reactive Oxygen Species 42-45 angiotensinogen Homo sapiens 83-89 30338935-5 2019 In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling. Reactive Oxygen Species 76-99 angiotensinogen Homo sapiens 45-51 30338935-5 2019 In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling. Reactive Oxygen Species 101-104 angiotensinogen Homo sapiens 45-51 30338935-5 2019 In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling. Reactive Oxygen Species 191-194 angiotensinogen Homo sapiens 45-51 30338935-7 2019 Thus, cardiac-specific Mst1 knockout inhibits ROS-mediated JNK signalling to block Ang II-induced cardiomyocyte apoptosis, suggesting Mst1 as a potential therapeutic target for treatment of RAAS-activated heart failure. Reactive Oxygen Species 46-49 angiotensinogen Homo sapiens 83-89 29977005-0 2018 ClC-3 promotes angiotensin II-induced reactive oxygen species production in endothelial cells by facilitating Nox2 NADPH oxidase complex formation. Reactive Oxygen Species 38-61 angiotensinogen Homo sapiens 15-29 30426047-3 2018 The data indicate that treatment with Angiotensin II and 6-OHDA increases the production of reactive oxygen species (ROS) and decreases cell viability. Reactive Oxygen Species 92-115 angiotensinogen Homo sapiens 38-52 30426047-3 2018 The data indicate that treatment with Angiotensin II and 6-OHDA increases the production of reactive oxygen species (ROS) and decreases cell viability. Reactive Oxygen Species 117-120 angiotensinogen Homo sapiens 38-52 29750475-2 2018 In sleep apnoea, a putative link between intermittent hypoxia and hypertension is the generation of oxygen radicals by angiotensin II and xanthine oxidase within the chemoreflex arc and vasculature. Reactive Oxygen Species 100-115 angiotensinogen Homo sapiens 119-133 29657902-0 2018 Inhibitory Effects of Angiotensin II Receptor Blockade on Human Tenon Fibroblast Migration and Reactive Oxygen Species Production in Cell Culture. Reactive Oxygen Species 95-118 angiotensinogen Homo sapiens 22-36 30002688-9 2018 Furthermore, apelin reduced AngII-induced ROS generation and enhanced telomerase activity in HUVECs (p < 0.05), which contributed to increased HUVEC viability as assessed by the CCK-8 assay (p < 0.05). Reactive Oxygen Species 42-45 angiotensinogen Homo sapiens 28-33 30002688-10 2018 Conclusions: The apelin/APJ axis improved AngII-induced HUVEC senescence via the AMPK/SIRT1 signaling pathway, and the underlying mechanisms might be associated with reduced ROS production and enhanced telomerase activity. Reactive Oxygen Species 174-177 angiotensinogen Homo sapiens 42-47 29361405-6 2018 Angiotensin (Ang) II, the main RAS effector peptide, has been shown to trigger significant upsurges in pro-inflammatory cytokines and reactive oxygen species (ROS). Reactive Oxygen Species 134-157 angiotensinogen Homo sapiens 0-20 29361405-6 2018 Angiotensin (Ang) II, the main RAS effector peptide, has been shown to trigger significant upsurges in pro-inflammatory cytokines and reactive oxygen species (ROS). Reactive Oxygen Species 159-162 angiotensinogen Homo sapiens 0-20 28600848-7 2018 Moreover, Ang II significantly increased the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and inflammatory cytokines (TNF-alpha and IL-1beta), reduced the levels of superoxide dismutase (SOD), glutathione (GSH), and these were reversed by Ad-DJ-1 transfection. Reactive Oxygen Species 55-78 angiotensinogen Homo sapiens 10-16 29359784-6 2018 In addition, Ang II significantly increased reactive oxygen species production and the levels of the inflammatory cytokine tumor necrosis factor-alpha and interleukin-6. Reactive Oxygen Species 44-67 angiotensinogen Homo sapiens 13-19 28600848-7 2018 Moreover, Ang II significantly increased the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and inflammatory cytokines (TNF-alpha and IL-1beta), reduced the levels of superoxide dismutase (SOD), glutathione (GSH), and these were reversed by Ad-DJ-1 transfection. Reactive Oxygen Species 80-83 angiotensinogen Homo sapiens 10-16 28916337-0 2017 Angiotensin II induces calcium-mediated autophagy in podocytes through enhancing reactive oxygen species levels. Reactive Oxygen Species 81-104 angiotensinogen Homo sapiens 0-14 29115506-0 2018 Angiotensin II induces monocyte chemoattractant protein-1 expression by increasing reactive oxygen species-mediated activation of the nuclear factor-kappaB signaling pathway in osteoblasts. Reactive Oxygen Species 83-106 angiotensinogen Homo sapiens 0-14 29115506-6 2018 The results of the present study ndicated that Ang II upregulated MCP-1 expression in osteoblasts, which was mitigated by agonists of the AT1R, including olmesartan, a ROS scavenger N-acetylcysteine (NAC), ammonium pyrrolidinethiocarbamate (PDTC) and nuclear factor (NF)-kappaB, but not by the Ang II type 2 receptor antagonist, PD123319. Reactive Oxygen Species 168-171 angiotensinogen Homo sapiens 47-53 29115506-7 2018 Furthermore, Ang II increased the generation of ROS and activated the NF-kappaB signaling pathway. Reactive Oxygen Species 48-51 angiotensinogen Homo sapiens 13-19 29115506-9 2018 In conclusion, these data indicated that Ang II enhanced ROS production and activated NF-kappaB signaling via AT1R, thus upregulating MCP-1 expression in osteoblasts. Reactive Oxygen Species 57-60 angiotensinogen Homo sapiens 41-47 28916337-15 2017 Consequently, this study demonstrated that Ang II could increase TRPC6 induced Ca2+ influx and enhance autophagy through increasing ROS levels in podocytes, and autophagy could protect Ang II-treated podocytes. Reactive Oxygen Species 132-135 angiotensinogen Homo sapiens 43-49 28916337-4 2017 The measurements of malondialdehyde (MDA) and H2O2 levels, and flow cytometry assay revealed that Ang II considerably increased reactive oxygen species (ROS) generation in podocytes. Reactive Oxygen Species 128-151 angiotensinogen Homo sapiens 98-104 28916337-4 2017 The measurements of malondialdehyde (MDA) and H2O2 levels, and flow cytometry assay revealed that Ang II considerably increased reactive oxygen species (ROS) generation in podocytes. Reactive Oxygen Species 153-156 angiotensinogen Homo sapiens 98-104 28916337-5 2017 Meaningfully, treatment with ROS scavenger N-(mercaptopropionyl)-glycine (N-MPG) could inhibit podocyte death and attenuate accumulation of ROS induced by Ang II. Reactive Oxygen Species 29-32 angiotensinogen Homo sapiens 155-161 28916337-5 2017 Meaningfully, treatment with ROS scavenger N-(mercaptopropionyl)-glycine (N-MPG) could inhibit podocyte death and attenuate accumulation of ROS induced by Ang II. Reactive Oxygen Species 140-143 angiotensinogen Homo sapiens 155-161 27658784-0 2016 The ROS derived mitochondrial respirstion not from NADPH oxidase plays key role in Celastrol against angiotensin II-mediated HepG2 cell proliferation. Reactive Oxygen Species 4-7 angiotensinogen Homo sapiens 101-115 27380400-5 2017 Activation of the Ang II type 1 (AT1) receptor pathway results in the production of proinflammatory mediators, intracellular formation of reactive oxygen species, cell proliferation, and extracellular matrix synthesis, which in turn facilities renal injury. Reactive Oxygen Species 138-161 angiotensinogen Homo sapiens 18-24 28259956-6 2017 Furthermore, hydrogen peroxide (H2O2; an exogenous ROS) downregulated the expression and activity of CSE, and had similar effects as AngII, whereas the inhibitory effects of AngII were completely suppressed by N-acetyl-L-cysteine (a ROS scavenger). Reactive Oxygen Species 51-54 angiotensinogen Homo sapiens 174-179 28259956-6 2017 Furthermore, hydrogen peroxide (H2O2; an exogenous ROS) downregulated the expression and activity of CSE, and had similar effects as AngII, whereas the inhibitory effects of AngII were completely suppressed by N-acetyl-L-cysteine (a ROS scavenger). Reactive Oxygen Species 233-236 angiotensinogen Homo sapiens 174-179 27695972-8 2017 Additionally, angiotensin II also stimulated the production of reactive oxygen species in RPE cells. Reactive Oxygen Species 63-86 angiotensinogen Homo sapiens 14-28 27356044-2 2017 The intracellular reactive oxygen species (ROS) leads to oxidative stress and it is raised from the mitochondria as well as by activation of five major pathways: increased polyol pathway flux, activation of protein kinase C (PKC) pathway, increased formation of advanced glycation end products (AGEs), over activity of hexosamine pathway and increased production of angiotensin II. Reactive Oxygen Species 18-41 angiotensinogen Homo sapiens 366-380 27356044-2 2017 The intracellular reactive oxygen species (ROS) leads to oxidative stress and it is raised from the mitochondria as well as by activation of five major pathways: increased polyol pathway flux, activation of protein kinase C (PKC) pathway, increased formation of advanced glycation end products (AGEs), over activity of hexosamine pathway and increased production of angiotensin II. Reactive Oxygen Species 43-46 angiotensinogen Homo sapiens 366-380 28871102-5 2017 Ang II decreased oxygen consumption rate, which resulted in reactive oxygen species (ROS) generation and inhibition of ROS blocked Ang II-mediated JNK phosphorylation and TGF-beta1 induction. Reactive Oxygen Species 60-83 angiotensinogen Homo sapiens 0-6 28871102-5 2017 Ang II decreased oxygen consumption rate, which resulted in reactive oxygen species (ROS) generation and inhibition of ROS blocked Ang II-mediated JNK phosphorylation and TGF-beta1 induction. Reactive Oxygen Species 85-88 angiotensinogen Homo sapiens 0-6 28871102-5 2017 Ang II decreased oxygen consumption rate, which resulted in reactive oxygen species (ROS) generation and inhibition of ROS blocked Ang II-mediated JNK phosphorylation and TGF-beta1 induction. Reactive Oxygen Species 119-122 angiotensinogen Homo sapiens 0-6 28871102-5 2017 Ang II decreased oxygen consumption rate, which resulted in reactive oxygen species (ROS) generation and inhibition of ROS blocked Ang II-mediated JNK phosphorylation and TGF-beta1 induction. Reactive Oxygen Species 119-122 angiotensinogen Homo sapiens 131-137 28363602-3 2017 We previously reported that angiotensin II (Ang II) and zinc increase reactive oxygen species (ROS) and cause senescence of vascular smooth muscle cells (VSMCs) and that senescence induced by Ang II is a zinc-dependent process. Reactive Oxygen Species 70-93 angiotensinogen Homo sapiens 28-42 28363602-3 2017 We previously reported that angiotensin II (Ang II) and zinc increase reactive oxygen species (ROS) and cause senescence of vascular smooth muscle cells (VSMCs) and that senescence induced by Ang II is a zinc-dependent process. Reactive Oxygen Species 70-93 angiotensinogen Homo sapiens 44-50 28363602-3 2017 We previously reported that angiotensin II (Ang II) and zinc increase reactive oxygen species (ROS) and cause senescence of vascular smooth muscle cells (VSMCs) and that senescence induced by Ang II is a zinc-dependent process. Reactive Oxygen Species 95-98 angiotensinogen Homo sapiens 28-42 28363602-3 2017 We previously reported that angiotensin II (Ang II) and zinc increase reactive oxygen species (ROS) and cause senescence of vascular smooth muscle cells (VSMCs) and that senescence induced by Ang II is a zinc-dependent process. Reactive Oxygen Species 95-98 angiotensinogen Homo sapiens 44-50 28259956-5 2017 The present study demonstrated that AngII not only upregulated the expression levels of inducible nitric oxide synthase (iNOS), stimulated ROS production and increased cell apoptosis, but also downregulated the expression levels of phosphorylated-endothelial nitric oxide synthase, decreased the expression and activity of cystathionine-c-lyase (CSE) and decreased cell viability. Reactive Oxygen Species 139-142 angiotensinogen Homo sapiens 36-41 28131837-5 2017 We also studied the effects of isohumulones on i) the cell viability under hypoxia and ii) the levels of angiotensin II (AT-II)-induced reactive oxygen species (ROS) in the cultured human aortic endothelial cells (HAECs). Reactive Oxygen Species 136-159 angiotensinogen Homo sapiens 105-119 28131837-5 2017 We also studied the effects of isohumulones on i) the cell viability under hypoxia and ii) the levels of angiotensin II (AT-II)-induced reactive oxygen species (ROS) in the cultured human aortic endothelial cells (HAECs). Reactive Oxygen Species 136-159 angiotensinogen Homo sapiens 121-126 28131837-5 2017 We also studied the effects of isohumulones on i) the cell viability under hypoxia and ii) the levels of angiotensin II (AT-II)-induced reactive oxygen species (ROS) in the cultured human aortic endothelial cells (HAECs). Reactive Oxygen Species 161-164 angiotensinogen Homo sapiens 105-119 28131837-5 2017 We also studied the effects of isohumulones on i) the cell viability under hypoxia and ii) the levels of angiotensin II (AT-II)-induced reactive oxygen species (ROS) in the cultured human aortic endothelial cells (HAECs). Reactive Oxygen Species 161-164 angiotensinogen Homo sapiens 121-126 28131837-9 2017 IHE also reduced the AT-II-induced intracellular ROS level. Reactive Oxygen Species 49-52 angiotensinogen Homo sapiens 21-26 28204818-0 2017 Reactive oxygen species mediate angiotensin II-induced transcytosis of low-density lipoprotein across endothelial cells. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 32-46 28204818-4 2017 In the present study, we found that Ang II upregulated intracellular reactive oxygen species (ROS) levels in endothelial cells (ECs) by measuring fluorescence of 2",7"-dichlorofluorescein (DCF-DA). Reactive Oxygen Species 69-92 angiotensinogen Homo sapiens 36-42 28204818-4 2017 In the present study, we found that Ang II upregulated intracellular reactive oxygen species (ROS) levels in endothelial cells (ECs) by measuring fluorescence of 2",7"-dichlorofluorescein (DCF-DA). Reactive Oxygen Species 94-97 angiotensinogen Homo sapiens 36-42 28204818-10 2017 Consequently, ROS are critical mediators in Ang II-induced LDL transcytosis. Reactive Oxygen Species 14-17 angiotensinogen Homo sapiens 44-50 28630660-4 2017 The effects of various NPC-EXs on angiotensin II- (Ang II-) induced reactive oxygen species (ROS) overproduction, apoptosis, and dysfunction, as well as dysregulation of Nox2, ephrin A3, VEGF, and p-VEGFR2/VEGFR2 in ECs were evaluated. Reactive Oxygen Species 68-91 angiotensinogen Homo sapiens 34-48 28630660-4 2017 The effects of various NPC-EXs on angiotensin II- (Ang II-) induced reactive oxygen species (ROS) overproduction, apoptosis, and dysfunction, as well as dysregulation of Nox2, ephrin A3, VEGF, and p-VEGFR2/VEGFR2 in ECs were evaluated. Reactive Oxygen Species 93-96 angiotensinogen Homo sapiens 34-48 27634835-9 2016 In vitro, vascular smooth muscle cells with small-interfering RNA knockdown of IMD showed significantly increased angiotensin II-induced reactive oxygen species, and small-interfering RNA knockdown of Nox4 markedly inhibited the reactive oxygen species. Reactive Oxygen Species 137-160 angiotensinogen Homo sapiens 114-128 27658784-4 2016 The results revealed that AngII was able to significantly promote HepG2 cell proliferation via up-regulating AngII type 1 (AT1) receptor expression, improving mitochondrial respiratory function, enhancing nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, increasing the levels of reactive oxygen species (ROS) and pro-inflammatory cytokines. Reactive Oxygen Species 300-323 angiotensinogen Homo sapiens 26-31 27658784-4 2016 The results revealed that AngII was able to significantly promote HepG2 cell proliferation via up-regulating AngII type 1 (AT1) receptor expression, improving mitochondrial respiratory function, enhancing nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, increasing the levels of reactive oxygen species (ROS) and pro-inflammatory cytokines. Reactive Oxygen Species 325-328 angiotensinogen Homo sapiens 26-31 27422988-9 2016 ROS activity, which was increased in endothelium of aging arteries, was also reduced by inhibiting ANG II (perindoprilat, losartan). Reactive Oxygen Species 0-3 angiotensinogen Homo sapiens 99-105 27352778-3 2016 Mechanistically, NADPH oxidase (NOX) is a multicomponent enzyme complex that is able to generate reactive oxygen species (ROS) as a downstream signaling pathway of Ang II which is expressed in liver. Reactive Oxygen Species 97-120 angiotensinogen Homo sapiens 164-170 27352778-3 2016 Mechanistically, NADPH oxidase (NOX) is a multicomponent enzyme complex that is able to generate reactive oxygen species (ROS) as a downstream signaling pathway of Ang II which is expressed in liver. Reactive Oxygen Species 122-125 angiotensinogen Homo sapiens 164-170 27381955-0 2016 Reactive oxygen species derived from NADPH oxidase 1 and mitochondria mediate angiotensin II-induced smooth muscle cell senescence. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 78-92 27381955-5 2016 Ang II (10(-7)M) stimulated ROS generation, exhibiting early increases between 30 and 60min and sustained increases between 24h and 72h, and induced VSMCs senescence after 48h or 72h treatment as assessed with senescence-associated beta-galactosidase activity and the expression of two cell cycle inhibitors, p21 and p16. Reactive Oxygen Species 28-31 angiotensinogen Homo sapiens 0-6 27381955-8 2016 Nox1 siRNA inhibited both early and sustained ROS increases induced by Ang II. Reactive Oxygen Species 46-49 angiotensinogen Homo sapiens 71-77 27381955-9 2016 In addition, a mitochondrial-specific antioxidant, mitoQ10, effectively inhibited Ang II-induced ROS increases and cellular senescence. Reactive Oxygen Species 97-100 angiotensinogen Homo sapiens 82-88 26728324-7 2016 In vitro, Ang II treatment elevated NOX4 protein expression and ROS production in hepatic stellate cells (HSCs), whereas it inhibited GSH and Nrf2-ARE, resulting in the activation of the NLRP3 inflammasome in the mitochondria of HSCs. Reactive Oxygen Species 64-67 angiotensinogen Homo sapiens 10-16 27570480-8 2016 DAPT also arrested the cell cycle progression in the G0/G1-phase, and attenuated calcium overload and ROS production caused by Ang II. Reactive Oxygen Species 102-105 angiotensinogen Homo sapiens 127-133 26728324-12 2016 INNOVATION AND CONCLUSIONS: Ang-(1-7) improved liver fibrosis by regulating NLRP3 inflammasome activation induced by Ang II-mediated ROS via redox balance modulation. Reactive Oxygen Species 133-136 angiotensinogen Homo sapiens 117-123 26746853-10 2016 CONCLUSIONS: Our results support that ANG-induced MCP-1 production in HUVECs is mediated by AT2 instead AT1 receptor activation, which in turn activates NF-kappaB involving reactive oxygen species produced by the NADPH oxidase complex. Reactive Oxygen Species 173-196 angiotensinogen Homo sapiens 38-41 26682942-7 2016 AngII potentiated the IL-1beta-mediated induction of NOX-1 expression, NADPH oxidase activity, ROS production, and cell migration. Reactive Oxygen Species 95-98 angiotensinogen Homo sapiens 0-5 26875562-6 2016 Treatment with hydrogen reduced Ang II- or AAC-induced oxidative stress, which was reflected by diminishing the induction of reactive oxygen species (ROS) in Ang II-stimulated VSMCs, inhibiting the levels of 3-nitrotyrosine (3-NT) in vascular and serum malondialdehyde (MDA). Reactive Oxygen Species 125-148 angiotensinogen Homo sapiens 32-38 26875562-6 2016 Treatment with hydrogen reduced Ang II- or AAC-induced oxidative stress, which was reflected by diminishing the induction of reactive oxygen species (ROS) in Ang II-stimulated VSMCs, inhibiting the levels of 3-nitrotyrosine (3-NT) in vascular and serum malondialdehyde (MDA). Reactive Oxygen Species 150-153 angiotensinogen Homo sapiens 32-38 27092079-10 2016 Ang II-induced ROS formation and upregulation of p22(phox) mRNA expression were inhibited by APN and NO. Reactive Oxygen Species 15-18 angiotensinogen Homo sapiens 0-6 26875562-8 2016 Taken together, our studies indicate that hydrogen prevents AAC-induced vascular hypertrophy in vivo, and inhibits Ang II-induced proliferation and migration of VSMCs in vitro possibly by targeting ROS-dependent ERK1/2, p38 MAPK, JNK and ERM signaling. Reactive Oxygen Species 198-201 angiotensinogen Homo sapiens 115-121 26779026-6 2015 This review will discuss the contribution of our laboratory and others regarding the sympathoexcitation caused by peripheral Ang-II-induced reactive oxygen species along the subfornical organ and paraventricular nucleus of the hypothalamus. Reactive Oxygen Species 140-163 angiotensinogen Homo sapiens 125-131 26696017-5 2016 Interestingly, in angiotensin-dependent hypertension, its beneficial effects on endothelial and kidney dysfunctions seem to at least in part be caused by its ability to decrease the levels of angiotensin II and increase angiotensin 1-7, in addition to improving nitric oxide bioavailability and diminishing reactive oxygen species. Reactive Oxygen Species 307-330 angiotensinogen Homo sapiens 192-235 26520903-1 2015 The effects of angiotensin II (Ang II) on vascular smooth muscle cells (VSMC) are modulated by reactive oxygen species (ROS) and also involve integrin engagement. Reactive Oxygen Species 95-118 angiotensinogen Homo sapiens 15-29 26520903-1 2015 The effects of angiotensin II (Ang II) on vascular smooth muscle cells (VSMC) are modulated by reactive oxygen species (ROS) and also involve integrin engagement. Reactive Oxygen Species 95-118 angiotensinogen Homo sapiens 31-37 26520903-1 2015 The effects of angiotensin II (Ang II) on vascular smooth muscle cells (VSMC) are modulated by reactive oxygen species (ROS) and also involve integrin engagement. Reactive Oxygen Species 120-123 angiotensinogen Homo sapiens 15-29 26520903-1 2015 The effects of angiotensin II (Ang II) on vascular smooth muscle cells (VSMC) are modulated by reactive oxygen species (ROS) and also involve integrin engagement. Reactive Oxygen Species 120-123 angiotensinogen Homo sapiens 31-37 26520903-5 2015 Ang II also stimulates ROS production in VSMC (140%) that is NOX1 dependent, being completely inhibited in NOX1 silenced cells. Reactive Oxygen Species 23-26 angiotensinogen Homo sapiens 0-6 25767030-1 2015 It is unclear if angiotensin II, which can increase the production of reactive oxygen species (oxidative stress), modulates heat loss responses of cutaneous blood flow and sweating. Reactive Oxygen Species 70-93 angiotensinogen Homo sapiens 17-31 26093296-3 2015 In this study, we found that angiotensin II dose-dependently increased the expression of Col1a1, Col3a1 and alpha-smooth muscle actin, which were blocked by ROS (reactive oxygen species) scavenger N-acetyl cysteine (NAC). Reactive Oxygen Species 157-160 angiotensinogen Homo sapiens 29-43 26093296-3 2015 In this study, we found that angiotensin II dose-dependently increased the expression of Col1a1, Col3a1 and alpha-smooth muscle actin, which were blocked by ROS (reactive oxygen species) scavenger N-acetyl cysteine (NAC). Reactive Oxygen Species 162-185 angiotensinogen Homo sapiens 29-43 26093296-4 2015 Mechanistically, angiotensin II induced robust ROS generation, which in turn induced cytoplasmic translocation of RNA binding protein HuR. Reactive Oxygen Species 47-50 angiotensinogen Homo sapiens 17-31 26093296-7 2015 Taken together, we here identified that angiotensin II promotes collagen synthesis in cardiac fibroblast through ROS-HuR-TGFbeta pathway. Reactive Oxygen Species 113-116 angiotensinogen Homo sapiens 40-54 25670255-0 2015 Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytes. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 52-66 25670255-10 2015 CONCLUSIONS: The positive inotropic response to 100nmol/L angiotensin II is due to both ROS/NHE-1 dependent and independent pathways, this being a point of divergence with the signaling previously described to be triggered by lower concentrations of angiotensin II (i.e.: 1nmol/L). Reactive Oxygen Species 88-91 angiotensinogen Homo sapiens 58-72 25770663-3 2015 Angiotensin II (Ang II) is a potent vasoactive agent that also exerts mitogenic, proinflammatory, and profibrotic effects through several signaling pathways, in part involving ROS, particularly superoxide and hydrogen peroxide. Reactive Oxygen Species 176-179 angiotensinogen Homo sapiens 0-14 25770663-3 2015 Angiotensin II (Ang II) is a potent vasoactive agent that also exerts mitogenic, proinflammatory, and profibrotic effects through several signaling pathways, in part involving ROS, particularly superoxide and hydrogen peroxide. Reactive Oxygen Species 176-179 angiotensinogen Homo sapiens 16-22 25770663-4 2015 Moreover, Ang II stimulates NADPH oxidases, leading to higher ROS generation and oxidative stress. Reactive Oxygen Species 62-65 angiotensinogen Homo sapiens 10-16 26101159-0 2015 Angiotensin-(1-7) counteracts angiotensin II-induced dysfunction in cerebral endothelial cells via modulating Nox2/ROS and PI3K/NO pathways. Reactive Oxygen Species 115-118 angiotensinogen Homo sapiens 30-44 26223796-3 2015 A key substance of renin-angiotensin-aldosterone system (RAAS), Angiotensin II (AngII) can induce cells dysfunction by increasing the production of ROS. Reactive Oxygen Species 148-151 angiotensinogen Homo sapiens 64-78 26223796-3 2015 A key substance of renin-angiotensin-aldosterone system (RAAS), Angiotensin II (AngII) can induce cells dysfunction by increasing the production of ROS. Reactive Oxygen Species 148-151 angiotensinogen Homo sapiens 80-85 26223796-8 2015 RESULTS: Here we show that AngII treatment could increase generation of ROS, and decrease eNOS activity and total level of NO, while upregulated eNOS expression as a compensatory mechanism. Reactive Oxygen Species 72-75 angiotensinogen Homo sapiens 27-32 26223796-11 2015 CONCLUSION: These data suggest that SIRT3 plays a role of protection in AngII-induced HUVECs dysfunction via regulation of ROS generation. Reactive Oxygen Species 123-126 angiotensinogen Homo sapiens 72-77 26184621-0 2015 From Contractile Enhancement to Pathological Hypertrophy: Angiotensin II-Induced Nox2-Mediated Reactive Oxygen Species. Reactive Oxygen Species 95-118 angiotensinogen Homo sapiens 58-72 25926752-6 2015 AngII also promotes podocyte injury through increased calcium influx and the generation of reactive oxygen species. Reactive Oxygen Species 91-114 angiotensinogen Homo sapiens 0-5 25757933-10 2015 In addition, benzbromarone inhibited reactive oxygen species production that was induced by angiotensin II or uric acid in endothelial cells. Reactive Oxygen Species 37-60 angiotensinogen Homo sapiens 92-106 25519738-5 2015 Intracellular signaling factors, such as protein kinase C (PKC), reactive oxygen species (ROS), and the mitogen-activated protein (MAP) kinase pathway, mediate the effects of central angiotensin II (ANG II). Reactive Oxygen Species 65-88 angiotensinogen Homo sapiens 183-197 25519738-5 2015 Intracellular signaling factors, such as protein kinase C (PKC), reactive oxygen species (ROS), and the mitogen-activated protein (MAP) kinase pathway, mediate the effects of central angiotensin II (ANG II). Reactive Oxygen Species 65-88 angiotensinogen Homo sapiens 199-205 25519738-5 2015 Intracellular signaling factors, such as protein kinase C (PKC), reactive oxygen species (ROS), and the mitogen-activated protein (MAP) kinase pathway, mediate the effects of central angiotensin II (ANG II). Reactive Oxygen Species 90-93 angiotensinogen Homo sapiens 183-197 25519738-5 2015 Intracellular signaling factors, such as protein kinase C (PKC), reactive oxygen species (ROS), and the mitogen-activated protein (MAP) kinase pathway, mediate the effects of central angiotensin II (ANG II). Reactive Oxygen Species 90-93 angiotensinogen Homo sapiens 199-205 25886843-0 2015 Qian Yang Yu Yin Granule-containing serum inhibits angiotensin II-induced proliferation, reactive oxygen species production, and inflammation in human mesangial cells via an NADPH oxidase 4-dependent pathway. Reactive Oxygen Species 89-112 angiotensinogen Homo sapiens 51-65 25886843-3 2015 METHODS: We hypothesize that QYYYG relieves hypertensive renal injury through an angiotensin II (Ang II)-nicotinamide adenine dinucleotide phosphate (NAPDH)-oxidase (NOX)-reactive oxygen species (ROS) pathway. Reactive Oxygen Species 171-194 angiotensinogen Homo sapiens 81-95 25886843-3 2015 METHODS: We hypothesize that QYYYG relieves hypertensive renal injury through an angiotensin II (Ang II)-nicotinamide adenine dinucleotide phosphate (NAPDH)-oxidase (NOX)-reactive oxygen species (ROS) pathway. Reactive Oxygen Species 171-194 angiotensinogen Homo sapiens 97-103 25886843-3 2015 METHODS: We hypothesize that QYYYG relieves hypertensive renal injury through an angiotensin II (Ang II)-nicotinamide adenine dinucleotide phosphate (NAPDH)-oxidase (NOX)-reactive oxygen species (ROS) pathway. Reactive Oxygen Species 196-199 angiotensinogen Homo sapiens 81-95 25886843-3 2015 METHODS: We hypothesize that QYYYG relieves hypertensive renal injury through an angiotensin II (Ang II)-nicotinamide adenine dinucleotide phosphate (NAPDH)-oxidase (NOX)-reactive oxygen species (ROS) pathway. Reactive Oxygen Species 196-199 angiotensinogen Homo sapiens 97-103 24327206-0 2014 Endogenous endothelin 1 mediates angiotensin II-induced hypertrophy in electrically paced cardiac myocytes through EGFR transactivation, reactive oxygen species and NHE-1. Reactive Oxygen Species 137-160 angiotensinogen Homo sapiens 33-47 25924472-5 2015 In addition, preincubation with crocetin resulted in a significant enhancement of cellular antioxidant capacity (P<0.05, P<0.01), while Ang II induced intracellular ROS decreased markedly (P<0.05, P<0.01). Reactive Oxygen Species 171-174 angiotensinogen Homo sapiens 142-148 25924472-6 2015 These results indicated that crocetin was capable of suppressing Ang II induced VCAM-1 expression and monocyte-endothelial cell adhesion by suppression of NF-kappaB activation, which might be derived from the enhancement of antioxidant capacity and subsequent reduction of intracellular ROS. Reactive Oxygen Species 287-290 angiotensinogen Homo sapiens 65-71 25078983-6 2014 Ang II induced HUVEC senescence and apoptosis, and increased ROS content and depolarization of MMP in a dose-dependent manner. Reactive Oxygen Species 61-64 angiotensinogen Homo sapiens 0-6 25534106-4 2014 AngII significantly increased ROS generation (1.70 +- 0.12 vs 1, P < 0.01), gene expression of collagen I,III both increased (1.31 +- 0.08 vs 1, 1.40 +- 0.09 vs 1, both P < 0.01) while MMP-1 decreased (0.68 +- 0.03 vs 1, P < 0.01). Reactive Oxygen Species 30-33 angiotensinogen Homo sapiens 0-5 25505418-7 2014 The binding of Ang II to AT1R activates NADPH oxidase, which leads to increased generation of cytoplasmic reactive oxygen species (ROS). Reactive Oxygen Species 106-129 angiotensinogen Homo sapiens 15-21 25505418-7 2014 The binding of Ang II to AT1R activates NADPH oxidase, which leads to increased generation of cytoplasmic reactive oxygen species (ROS). Reactive Oxygen Species 131-134 angiotensinogen Homo sapiens 15-21 25505418-8 2014 This Ang II-AT1R-NADPH-ROS signal triggers the opening of mitochondrial KATP channels and mitochondrial ROS production in a positive feedback loop. Reactive Oxygen Species 23-26 angiotensinogen Homo sapiens 5-11 25505418-8 2014 This Ang II-AT1R-NADPH-ROS signal triggers the opening of mitochondrial KATP channels and mitochondrial ROS production in a positive feedback loop. Reactive Oxygen Species 104-107 angiotensinogen Homo sapiens 5-11 25072659-0 2014 Hyperglycemia and angiotensin II cooperate to enhance collagen I deposition by cardiac fibroblasts through a ROS-STAT3-dependent mechanism. Reactive Oxygen Species 109-112 angiotensinogen Homo sapiens 18-32 25072659-3 2014 We observed that the diabetic environment 1) enhanced tyrosine phosphorylation of JAK2 and STAT3; 2) induced nuclear localization of tyrosine phosphorylated STAT3 through a reactive oxygen species-mediated mechanism, with angiotensin II stimulation further enhancing STAT3 nuclear accumulation; and 3) stimulated collagen I production. Reactive Oxygen Species 173-196 angiotensinogen Homo sapiens 222-236 26312151-6 2014 Transforming growth factor (TGF)-beta1 and reactive oxygen species (ROS) are the key mediators of the pro-fibrotic effect of Ang II causing apoptosis and epithelial-to-mesenchymal transition of the renal tubular epithelium. Reactive Oxygen Species 43-66 angiotensinogen Homo sapiens 125-131 26312151-6 2014 Transforming growth factor (TGF)-beta1 and reactive oxygen species (ROS) are the key mediators of the pro-fibrotic effect of Ang II causing apoptosis and epithelial-to-mesenchymal transition of the renal tubular epithelium. Reactive Oxygen Species 68-71 angiotensinogen Homo sapiens 125-131 26312151-8 2014 Other mechanisms of Ang II-induced fibrosis include ROS-dependent activation of hypoxia-inducible factor-1. Reactive Oxygen Species 52-55 angiotensinogen Homo sapiens 20-26 24940409-4 2014 Furthermore, we studied whether TFPN could attenuate the Ang II-induced generation of ROS and the activation of nuclear factor-kappaB (NF-kappaB); whether these Ang II-induced effects were inhibited by apocynin (a nicotinamide adenine dinucleotide phosphate oxidase inhibitor) and pyrrolidine dithiocarbamate (an NF-kappaB inhibitor). Reactive Oxygen Species 86-89 angiotensinogen Homo sapiens 57-63 24442713-0 2014 Angiotensin II-derived reactive oxygen species promote angiogenesis in human late endothelial progenitor cells through heme oxygenase-1 via ERK1/2 and AKT/PI3K pathways. Reactive Oxygen Species 23-46 angiotensinogen Homo sapiens 0-14 24442713-3 2014 We observed that Ang II could increase reactive oxygen species (ROS) and promote capillary formation in late EPCs. Reactive Oxygen Species 39-62 angiotensinogen Homo sapiens 17-23 24442713-3 2014 We observed that Ang II could increase reactive oxygen species (ROS) and promote capillary formation in late EPCs. Reactive Oxygen Species 64-67 angiotensinogen Homo sapiens 17-23 24442713-4 2014 Ang II-derived ROS could also upregulate heme oxygenase-1 (HO-1) expression, and treating late EPCs with HO-1 small interfering RNA or heme oxygenase inhibitor (HO inhibitor) could inhibit Ang II-induced tube formation and increase ROS level and apoptosis rate. Reactive Oxygen Species 15-18 angiotensinogen Homo sapiens 0-6 24442713-4 2014 Ang II-derived ROS could also upregulate heme oxygenase-1 (HO-1) expression, and treating late EPCs with HO-1 small interfering RNA or heme oxygenase inhibitor (HO inhibitor) could inhibit Ang II-induced tube formation and increase ROS level and apoptosis rate. Reactive Oxygen Species 15-18 angiotensinogen Homo sapiens 189-195 24442713-4 2014 Ang II-derived ROS could also upregulate heme oxygenase-1 (HO-1) expression, and treating late EPCs with HO-1 small interfering RNA or heme oxygenase inhibitor (HO inhibitor) could inhibit Ang II-induced tube formation and increase ROS level and apoptosis rate. Reactive Oxygen Species 232-235 angiotensinogen Homo sapiens 0-6 24442713-4 2014 Ang II-derived ROS could also upregulate heme oxygenase-1 (HO-1) expression, and treating late EPCs with HO-1 small interfering RNA or heme oxygenase inhibitor (HO inhibitor) could inhibit Ang II-induced tube formation and increase ROS level and apoptosis rate. Reactive Oxygen Species 232-235 angiotensinogen Homo sapiens 189-195 24442713-6 2014 Accordingly, Ang II-derived ROS could promote angiogenesis in late EPCs by inducing HO-1 expression via ERK1/2 and AKT/PI3K pathways, and we believe HO-1 might be a promising intervention target in EPCs due to its potent proangiogenic, antioxidant, and antiapoptosis potentials. Reactive Oxygen Species 28-31 angiotensinogen Homo sapiens 13-19 24976907-4 2014 Several vasoconstrictor peptides, such as angiotensin II, endothelin-1 and urotensin II, act through their receptors to stimulate the production of reactive oxygen species, by activating enzymes like NADPH oxidase and xanthine oxidase. Reactive Oxygen Species 148-171 angiotensinogen Homo sapiens 42-56 24940409-0 2014 Total flavonoids from Plumula Nelumbinis suppress angiotensin II-induced fractalkine production by inhibiting the ROS/NF-kappaB pathway in human umbilical vein endothelial cells. Reactive Oxygen Species 114-117 angiotensinogen Homo sapiens 50-64 24940409-1 2014 Angiotensin II (Ang II) is a neuroendocrine factor that promotes hypertension and has been implicated in vascular inflammation through the induction of reactive oxygen species (ROS) and proinflammatory genes in endothelial cells. Reactive Oxygen Species 152-175 angiotensinogen Homo sapiens 0-14 24940409-1 2014 Angiotensin II (Ang II) is a neuroendocrine factor that promotes hypertension and has been implicated in vascular inflammation through the induction of reactive oxygen species (ROS) and proinflammatory genes in endothelial cells. Reactive Oxygen Species 152-175 angiotensinogen Homo sapiens 16-22 24940409-1 2014 Angiotensin II (Ang II) is a neuroendocrine factor that promotes hypertension and has been implicated in vascular inflammation through the induction of reactive oxygen species (ROS) and proinflammatory genes in endothelial cells. Reactive Oxygen Species 177-180 angiotensinogen Homo sapiens 0-14 24940409-1 2014 Angiotensin II (Ang II) is a neuroendocrine factor that promotes hypertension and has been implicated in vascular inflammation through the induction of reactive oxygen species (ROS) and proinflammatory genes in endothelial cells. Reactive Oxygen Species 177-180 angiotensinogen Homo sapiens 16-22 24940409-6 2014 Furthermore, TFPN attenuated the Ang II-induced generation of ROS and the activation of nuclear factor-kappaB (NF-kappaB); these Ang II-induced effects were also inhibited by apocynin (a nicotinamide adenine dinucleotide phosphate oxidase inhibitor) and pyrrolidine dithiocarbamate (an NF-kappaB inhibitor). Reactive Oxygen Species 62-65 angiotensinogen Homo sapiens 33-39 24940409-7 2014 In conclusion, the findings of the present study indicate that TFPN attenuate Ang II-induced upregulation of FKN by inhibiting the ROS/NF-kappaB pathway in HUVECs and thus have a suppressive effect on vascular inflammation. Reactive Oxygen Species 131-134 angiotensinogen Homo sapiens 78-84 24262797-5 2014 Stimulation with angiotensin II upregulated Nox5 expression in human podocyte cultures and increased reactive oxygen species generation. Reactive Oxygen Species 101-124 angiotensinogen Homo sapiens 17-31 24262797-6 2014 siRNA-mediated Nox5 knockdown inhibited angiotensin II-stimulated production of reactive oxygen species and altered podocyte cytoskeletal dynamics, resulting in an Rac-mediated motile phenotype. Reactive Oxygen Species 80-103 angiotensinogen Homo sapiens 40-54 24592256-5 2014 The primary effector hormone of the RAS, angiotensin II, stimulates reactive oxygen species, induces tissue damage, and can be associated to most diabetic complications. Reactive Oxygen Species 68-91 angiotensinogen Homo sapiens 41-55 24484748-9 2014 In addition to its well-known role in hemodynamics, angiotensin II promotes activations of profibrogenic and inflammatory factors and cells and stimulates reactive oxygen species generation. Reactive Oxygen Species 155-178 angiotensinogen Homo sapiens 52-66 24493689-9 2013 The main mediators of skeletal muscle wasting in cancer are proteolysis-inducing factor (PIF), proinflammatory cytokines, and angiotensin II acting through increased levels of reactive oxygen species (ROS) and nuclear factor NF-kappaB activation, as well as glucocorticoid activated FOXO transcription factors and myostatin. Reactive Oxygen Species 176-199 angiotensinogen Homo sapiens 126-140 24392165-9 2014 Results showed 1) EPC-MVs were able to protect CMs against Ang II-induced changes in cell viability, apoptosis, surface area, beta-MHC expression and ROS over-production; 2) The effects were accompanied with the up-regulation of Akt/p-Akt and its downstream eNOS/p-eNOS, and were abolished by PI3K inhibition or partially blocked by NOS inhibition; 3) Depletion of RNAs from EPC-MVs partially or totally eliminated the effects of EPC-MVs. Reactive Oxygen Species 150-153 angiotensinogen Homo sapiens 59-65 24317407-6 2014 Following a myocardial infarction, pro-inflammatory cytokines in the paraventricular nucleus and the subsequent generation of reactive oxygen species, via angiotensin II activation of the angiotensin II type 1 receptor, increase neuronal excitability further, leading to sympathetic excitation. Reactive Oxygen Species 126-149 angiotensinogen Homo sapiens 155-169 24493689-9 2013 The main mediators of skeletal muscle wasting in cancer are proteolysis-inducing factor (PIF), proinflammatory cytokines, and angiotensin II acting through increased levels of reactive oxygen species (ROS) and nuclear factor NF-kappaB activation, as well as glucocorticoid activated FOXO transcription factors and myostatin. Reactive Oxygen Species 201-204 angiotensinogen Homo sapiens 126-140 24284398-2 2013 In rodent models, it has been reported that reactive oxygen species (ROS) are important for intrarenal angiotensinogen (AGT) augmentation in the progression of diabetic nephropathy. Reactive Oxygen Species 44-67 angiotensinogen Homo sapiens 103-118 23851032-10 2013 This chronic NF-kappaB activation is contributed by increased angiotensin-II signaling and downregulated sirtuins and precludes adequate cellular response to acute ROS generation. Reactive Oxygen Species 164-167 angiotensinogen Homo sapiens 62-76 24284398-2 2013 In rodent models, it has been reported that reactive oxygen species (ROS) are important for intrarenal angiotensinogen (AGT) augmentation in the progression of diabetic nephropathy. Reactive Oxygen Species 44-67 angiotensinogen Homo sapiens 120-123 24284398-2 2013 In rodent models, it has been reported that reactive oxygen species (ROS) are important for intrarenal angiotensinogen (AGT) augmentation in the progression of diabetic nephropathy. Reactive Oxygen Species 69-72 angiotensinogen Homo sapiens 103-118 24284398-2 2013 In rodent models, it has been reported that reactive oxygen species (ROS) are important for intrarenal angiotensinogen (AGT) augmentation in the progression of diabetic nephropathy. Reactive Oxygen Species 69-72 angiotensinogen Homo sapiens 120-123 23994555-2 2013 Angiotensin II (Ang II) can cause endothelial dysfunction by promoting intracellular ROS generation. Reactive Oxygen Species 85-88 angiotensinogen Homo sapiens 0-14 24363997-2 2013 AngII intra-neuronal signaling is mediated, at least in part, by reactive oxygen species, particularly superoxide (O2 ( -)). Reactive Oxygen Species 65-88 angiotensinogen Homo sapiens 0-5 23994555-2 2013 Angiotensin II (Ang II) can cause endothelial dysfunction by promoting intracellular ROS generation. Reactive Oxygen Species 85-88 angiotensinogen Homo sapiens 16-22 23994555-7 2013 Ang II significantly enhanced intracellular ROS levels, caused mitochondrial membrane dysfunction, and decreased cell viability, leading to apoptosis. Reactive Oxygen Species 44-47 angiotensinogen Homo sapiens 0-6 23940049-7 2013 Ang II also elicits an increase in mitochondrial abundance of Nox4 protein, and the oxidase contributes to ROS production in mitochondria. Reactive Oxygen Species 107-110 angiotensinogen Homo sapiens 0-6 23940049-8 2013 Overexpression of mitochondrial manganese superoxide dismutase prevents the stimulatory effects of Ang II on mitochondrial ROS production, loss of NO availability, and MC fibronectin accumulation, whereas manganese superoxide dismutase depletion increases mitochondrial ROS, NO deficiency, and fibronectin synthesis basally and in cells exposed to Ang II. Reactive Oxygen Species 123-126 angiotensinogen Homo sapiens 99-105 23940049-2 2013 Here, we demonstrate that, in MCs, Ang II induces endothelial nitric-oxide synthase (eNOS) uncoupling with enhanced generation of reactive oxygen species (ROS) and decreased production of NO. Reactive Oxygen Species 130-153 angiotensinogen Homo sapiens 35-41 23940049-8 2013 Overexpression of mitochondrial manganese superoxide dismutase prevents the stimulatory effects of Ang II on mitochondrial ROS production, loss of NO availability, and MC fibronectin accumulation, whereas manganese superoxide dismutase depletion increases mitochondrial ROS, NO deficiency, and fibronectin synthesis basally and in cells exposed to Ang II. Reactive Oxygen Species 270-273 angiotensinogen Homo sapiens 99-105 23940049-2 2013 Here, we demonstrate that, in MCs, Ang II induces endothelial nitric-oxide synthase (eNOS) uncoupling with enhanced generation of reactive oxygen species (ROS) and decreased production of NO. Reactive Oxygen Species 155-158 angiotensinogen Homo sapiens 35-41 22530599-3 2013 The diverse actions of Ang II are mediated via Ang II type 1 and Ang II type 2 receptors, which couple to various signaling molecules, including NADPH oxidase (Nox), which generates reactive oxygen species (ROS). Reactive Oxygen Species 207-210 angiotensinogen Homo sapiens 47-53 22530599-4 2013 ROS are now recognized as signaling molecules, critically placed in pathways activated by Ang II. Reactive Oxygen Species 0-3 angiotensinogen Homo sapiens 90-96 22530599-6 2013 RECENT ADVANCES: Ang II regulates vascular cell production of ROS through various recently characterized Noxs, including Nox1, Nox2, Nox4, and Nox5. Reactive Oxygen Species 62-65 angiotensinogen Homo sapiens 17-23 22429119-2 2013 One of the most promising theses that emerged during the last decade is that production of reactive oxygen species (ROS) and activation of redox-dependent signaling cascades underlie those Ang II actions. Reactive Oxygen Species 91-114 angiotensinogen Homo sapiens 189-195 22429119-2 2013 One of the most promising theses that emerged during the last decade is that production of reactive oxygen species (ROS) and activation of redox-dependent signaling cascades underlie those Ang II actions. Reactive Oxygen Species 116-119 angiotensinogen Homo sapiens 189-195 22530599-7 2013 Activation of these Noxs leads to ROS generation, which in turn influences many downstream signaling targets of Ang II, including MAP kinases, RhoA/Rho kinase, transcription factors, protein tyrosine phosphatases, and tyrosine kinases. Reactive Oxygen Species 34-37 angiotensinogen Homo sapiens 112-118 22429119-3 2013 This review summarizes our status of understanding on the roles of ROS and redox-sensitive signaling in brain Ang II-dependent cardiovascular diseases, using hypertension and heart failure as illustrative examples. Reactive Oxygen Species 67-70 angiotensinogen Homo sapiens 110-116 22530599-9 2013 CRITICAL ISSUES: Although there is much evidence indicating a role for Nox/ROS in Ang II function, there is still a paucity of information on how Ang II exerts cell-specific effects through ROS and how Nox isoforms are differentially regulated by Ang II. Reactive Oxygen Species 75-78 angiotensinogen Homo sapiens 82-88 22429119-4 2013 RECENT ADVANCES: ROS generated by NADPH oxidase, mitochondrial electron transport chain, and proinflammatory cytokines activates mitogen-activated protein kinases and transcription factors, which in turn modulate ion channel functions and ultimately increase neuronal activity and sympathetic outflow in brain Ang II-dependent cardiovascular diseases. Reactive Oxygen Species 17-20 angiotensinogen Homo sapiens 310-316 22429119-5 2013 Antioxidants targeting ROS have been demonstrated to be beneficial to Ang II-induced hypertension and heart failure via protection from oxidative stress in brain regions that subserve cardiovascular regulation. Reactive Oxygen Species 23-26 angiotensinogen Homo sapiens 70-76 22530599-10 2013 Moreover, exact mechanisms whereby ROS induce oxidative modifications of signaling molecules mediating Ang II actions remain elusive. Reactive Oxygen Species 35-38 angiotensinogen Homo sapiens 103-109 23868084-1 2013 OBJECTIVE: Oxidative stress has been linked to endothelial dysfunction and angiotensin II stimulates the reactive oxygen species production contributing to several cardiovascular diseases. Reactive Oxygen Species 105-128 angiotensinogen Homo sapiens 75-89 22443458-0 2013 Angiotensin II-induced production of mitochondrial reactive oxygen species: potential mechanisms and relevance for cardiovascular disease. Reactive Oxygen Species 51-74 angiotensinogen Homo sapiens 0-14 22443458-1 2013 SIGNIFICANCE: The role of reactive oxygen species (ROS) in angiotensin II (AngII) induced endothelial dysfunction, cardiovascular and renal remodeling, inflammation, and fibrosis has been well documented. Reactive Oxygen Species 26-49 angiotensinogen Homo sapiens 59-73 22443458-1 2013 SIGNIFICANCE: The role of reactive oxygen species (ROS) in angiotensin II (AngII) induced endothelial dysfunction, cardiovascular and renal remodeling, inflammation, and fibrosis has been well documented. Reactive Oxygen Species 26-49 angiotensinogen Homo sapiens 75-80 22443458-1 2013 SIGNIFICANCE: The role of reactive oxygen species (ROS) in angiotensin II (AngII) induced endothelial dysfunction, cardiovascular and renal remodeling, inflammation, and fibrosis has been well documented. Reactive Oxygen Species 51-54 angiotensinogen Homo sapiens 59-73 22443458-1 2013 SIGNIFICANCE: The role of reactive oxygen species (ROS) in angiotensin II (AngII) induced endothelial dysfunction, cardiovascular and renal remodeling, inflammation, and fibrosis has been well documented. Reactive Oxygen Species 51-54 angiotensinogen Homo sapiens 75-80 22443458-3 2013 AngII also increases the production of mitochondrial ROS, while the inhibition of AngII improves mitochondrial function; however, the specific molecular mechanisms of the stimulation of mitochondrial ROS is not clear. Reactive Oxygen Species 53-56 angiotensinogen Homo sapiens 0-5 22443458-3 2013 AngII also increases the production of mitochondrial ROS, while the inhibition of AngII improves mitochondrial function; however, the specific molecular mechanisms of the stimulation of mitochondrial ROS is not clear. Reactive Oxygen Species 200-203 angiotensinogen Homo sapiens 0-5 22443458-4 2013 RECENT ADVANCES: Interestingly, the overexpression of mitochondrial thioredoxin 2 or mitochondrial superoxide dismutase attenuates AngII-induced hypertension, which demonstrates the importance of mitochondrial ROS in AngII-mediated cardiovascular diseases. Reactive Oxygen Species 210-213 angiotensinogen Homo sapiens 131-136 22443458-4 2013 RECENT ADVANCES: Interestingly, the overexpression of mitochondrial thioredoxin 2 or mitochondrial superoxide dismutase attenuates AngII-induced hypertension, which demonstrates the importance of mitochondrial ROS in AngII-mediated cardiovascular diseases. Reactive Oxygen Species 210-213 angiotensinogen Homo sapiens 217-222 22443458-5 2013 CRITICAL ISSUES: Although mitochondrial ROS plays an important role in normal physiological cell signaling, AngII, high glucose, high fat, or hypoxia may cause the overproduction of mitochondrial ROS, leading to the feed-forward redox stimulation of NADPH oxidases. Reactive Oxygen Species 196-199 angiotensinogen Homo sapiens 108-113 22530599-3 2013 The diverse actions of Ang II are mediated via Ang II type 1 and Ang II type 2 receptors, which couple to various signaling molecules, including NADPH oxidase (Nox), which generates reactive oxygen species (ROS). Reactive Oxygen Species 182-205 angiotensinogen Homo sapiens 23-29 22530599-3 2013 The diverse actions of Ang II are mediated via Ang II type 1 and Ang II type 2 receptors, which couple to various signaling molecules, including NADPH oxidase (Nox), which generates reactive oxygen species (ROS). Reactive Oxygen Species 182-205 angiotensinogen Homo sapiens 47-53 22530599-3 2013 The diverse actions of Ang II are mediated via Ang II type 1 and Ang II type 2 receptors, which couple to various signaling molecules, including NADPH oxidase (Nox), which generates reactive oxygen species (ROS). Reactive Oxygen Species 182-205 angiotensinogen Homo sapiens 47-53 22530599-3 2013 The diverse actions of Ang II are mediated via Ang II type 1 and Ang II type 2 receptors, which couple to various signaling molecules, including NADPH oxidase (Nox), which generates reactive oxygen species (ROS). Reactive Oxygen Species 207-210 angiotensinogen Homo sapiens 23-29 22530599-3 2013 The diverse actions of Ang II are mediated via Ang II type 1 and Ang II type 2 receptors, which couple to various signaling molecules, including NADPH oxidase (Nox), which generates reactive oxygen species (ROS). Reactive Oxygen Species 207-210 angiotensinogen Homo sapiens 47-53 23769949-5 2013 Ang II activates the ubiquitin-proteasome system via generation of reactive oxygen species and via inhibition of the insulin-like growth factor-1 signaling pathway. Reactive Oxygen Species 67-90 angiotensinogen Homo sapiens 0-6 23846495-1 2013 OBJECTIVE: Angiotensin II (AngII) signal transduction in vascular smooth muscle cells (VSMC) is mediated by reactive oxygen species (ROS). Reactive Oxygen Species 108-131 angiotensinogen Homo sapiens 27-32 23846495-1 2013 OBJECTIVE: Angiotensin II (AngII) signal transduction in vascular smooth muscle cells (VSMC) is mediated by reactive oxygen species (ROS). Reactive Oxygen Species 133-136 angiotensinogen Homo sapiens 11-25 23846495-1 2013 OBJECTIVE: Angiotensin II (AngII) signal transduction in vascular smooth muscle cells (VSMC) is mediated by reactive oxygen species (ROS). Reactive Oxygen Species 108-131 angiotensinogen Homo sapiens 11-25 23846495-1 2013 OBJECTIVE: Angiotensin II (AngII) signal transduction in vascular smooth muscle cells (VSMC) is mediated by reactive oxygen species (ROS). Reactive Oxygen Species 133-136 angiotensinogen Homo sapiens 27-32 23846495-2 2013 Cyclophilin A (CyPA) is a ubiquitously expressed cytosolic protein that possesses peptidyl-prolyl cis-trans isomerase activity, scaffold function, and significantly enhances AngII-induced ROS production in VSMC. Reactive Oxygen Species 188-191 angiotensinogen Homo sapiens 174-179 23846495-3 2013 We hypothesized that CyPA regulates AngII-induced ROS generation by promoting translocation of NADPH oxidase cytosolic subunit p47phox to caveolae of the plasma membrane. Reactive Oxygen Species 50-53 angiotensinogen Homo sapiens 36-41 23846495-4 2013 APPROACH AND RESULTS: Overexpression of CyPA in CyPA-deficient VSMC (CyPA(-/-)VSMC) significantly increased AngII-stimulated ROS production. Reactive Oxygen Species 125-128 angiotensinogen Homo sapiens 108-113 23846495-5 2013 Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitors (VAS2870 or diphenylene iodonium) significantly attenuated AngII-induced ROS production in CyPA and p47phox-overexpressing CyPA(-/-)VSMC. Reactive Oxygen Species 144-147 angiotensinogen Homo sapiens 130-135 23846495-12 2013 CONCLUSIONS: These findings provide the mechanism by which CyPA is an important regulator for AngII-induced ROS generation in VSMC through interaction with p47phox and cell cytoskeleton, which enhances the translocation of p47phox to caveolae. Reactive Oxygen Species 108-111 angiotensinogen Homo sapiens 94-99 23261942-3 2013 Because reactive oxygen species play a role both in inflammation and in the cellular signaling pathway of Ang II, the appearance of protein adducts of the "second messenger of free radicals," the aldehyde 4-hydroxynonenal (HNE), in otosclerotic bone has been analyzed. Reactive Oxygen Species 8-31 angiotensinogen Homo sapiens 106-112 24417152-7 2013 RESULTS: Compared with control group, Ang II could increase the level of ROS, inhibit cytochrome activity and enhance caspase 3 expression in HUVECs, as a result, enhance apoptosis of HUVECs. Reactive Oxygen Species 73-76 angiotensinogen Homo sapiens 38-44 24417152-9 2013 CONCLUSION: HSYA can eliminate the effect of Ang II and its mechanism may be related to inhibiting ROS producing, keeping mitochondrial structure and function and inhibiting apoptosis. Reactive Oxygen Species 99-102 angiotensinogen Homo sapiens 45-51 23875251-0 2013 Nifedipine inhibits angiotensin II-induced cardiac fibrosis via downregulating Nox4-derived ROS generation and suppressing ERK1/2, JNK signaling pathways. Reactive Oxygen Species 92-95 angiotensinogen Homo sapiens 20-34 23717285-0 2013 Angiotensin-II-derived reactive oxygen species on baroreflex sensitivity during hypertension: new perspectives. Reactive Oxygen Species 23-46 angiotensinogen Homo sapiens 0-14 23548909-6 2013 In the presence of these vesicles, angiotensin II-induced production of reactive oxygen species (ROS) was considerably enhanced. Reactive Oxygen Species 72-95 angiotensinogen Homo sapiens 35-49 23548909-6 2013 In the presence of these vesicles, angiotensin II-induced production of reactive oxygen species (ROS) was considerably enhanced. Reactive Oxygen Species 97-100 angiotensinogen Homo sapiens 35-49 23548909-8 2013 Angiotensin II-induced ROS decreased the bioavailability of eNOS under the FC-enriched condition. Reactive Oxygen Species 23-26 angiotensinogen Homo sapiens 0-14 26105877-4 2013 Binding of Angiotensin II to its type I receptor (AT1R) increases generation of reactive oxygen species and we have shown an increase in AT1R in PE [2]. Reactive Oxygen Species 80-103 angiotensinogen Homo sapiens 11-25 23348709-4 2013 Coenzyme Q10 (10muM) prevented the actions of angiotensin II (100nM): overproduction of reactive oxygen species, increases in expression of p22(phox) and Nox2 subunits of NADPH oxidase, and inhibition of insulin-induced nitric oxide production. Reactive Oxygen Species 88-111 angiotensinogen Homo sapiens 46-60 23316164-6 2012 In the cerebral circulation, Ang II has been implicated in reactive oxygen species generation, alterations to vasomotor function, impaired neurovascular coupling, inflammation, and vascular remodeling. Reactive Oxygen Species 59-82 angiotensinogen Homo sapiens 29-35 22569796-6 2012 Meanwhile, choline pretreatment prevented the augment of reactive oxygen species (ROS) and intracellular calcium concentration in Ang II-treated cardiomyocytes. Reactive Oxygen Species 57-80 angiotensinogen Homo sapiens 130-136 24021937-0 2013 Angiotensin II induces C-reactive protein expression via AT1-ROS-MAPK-NF-kappaB signal pathway in hepatocytes. Reactive Oxygen Species 61-64 angiotensinogen Homo sapiens 0-14 24021937-10 2013 Losartan and thenoyltrifluoroacetone decreased Ang II-stimulated ROS production. Reactive Oxygen Species 65-68 angiotensinogen Homo sapiens 47-53 24021937-15 2013 CONCLUSION: Ang II has ability to induce CRP expression in hepatocytes in vitro and in vivo through AT1 receptor followed by ROS, MAPK and NF-kappaB signal pathway. Reactive Oxygen Species 125-128 angiotensinogen Homo sapiens 12-18 23045460-9 2012 Taken together, these data demonstrate that inhibition of mitochondrial reactive oxygen species attenuates angiotensin II-induced hypertension and corrects the imbalance in EPCs/ICs in the BM. Reactive Oxygen Species 72-95 angiotensinogen Homo sapiens 107-121 22659808-5 2012 METHODS: HAECs were cultured, and Ang II (10(-6) M) was used as a stimulant for the generation of CRP and reactive oxygen species (ROS). Reactive Oxygen Species 106-129 angiotensinogen Homo sapiens 34-40 22659808-5 2012 METHODS: HAECs were cultured, and Ang II (10(-6) M) was used as a stimulant for the generation of CRP and reactive oxygen species (ROS). Reactive Oxygen Species 131-134 angiotensinogen Homo sapiens 34-40 22659808-10 2012 Meanwhile, AT(1) receptor blocker losartan also reduced Ang II-stimulated ROS generation in HAECs (P < 0.001 vs. Ang II alone). Reactive Oxygen Species 74-77 angiotensinogen Homo sapiens 56-62 22659808-11 2012 CONCLUSIONS: Rosiglitazone at the concentrations used in the present experiment is able to inhibit Ang II-induced CRP generation in HAECs by regulating AT(1)-ROS-MAPK signal pathway. Reactive Oxygen Species 158-161 angiotensinogen Homo sapiens 99-105 23012797-3 2012 Angiotensin II stimulates the production of reactive oxygen species by the activation of NADPH oxidase and increases Rho-associated kinase activity that decreases the stability of endothelial nitric oxide synthase (eNOS) mRNA and phosphorylation of eNOS, leading to inactivation of NO bioavailability. Reactive Oxygen Species 44-67 angiotensinogen Homo sapiens 0-14 23012797-4 2012 An imbalance of reduced production of NO or increased production of reactive oxygen species may promote endothelial cell dysfunction through angiotensin II-induced various signal transduction cascades. Reactive Oxygen Species 68-91 angiotensinogen Homo sapiens 141-155 22798525-0 2012 Phosphorylation of smooth muscle 22alpha facilitates angiotensin II-induced ROS production via activation of the PKCdelta-P47phox axis through release of PKCdelta and actin dynamics and is associated with hypertrophy and hyperplasia of vascular smooth muscle cells in vitro and in vivo. Reactive Oxygen Species 76-79 angiotensinogen Homo sapiens 53-67 24587981-2 2012 Ang II is the principle effector of the renin-angiotensin system for maintaining homeostasis in the cardiovascular system, as well as a potent stimulator of NAD(P)H oxidase, which is the major source and primary trigger for reactive oxygen species (ROS) generation in various tissues. Reactive Oxygen Species 224-247 angiotensinogen Homo sapiens 0-6 24587981-2 2012 Ang II is the principle effector of the renin-angiotensin system for maintaining homeostasis in the cardiovascular system, as well as a potent stimulator of NAD(P)H oxidase, which is the major source and primary trigger for reactive oxygen species (ROS) generation in various tissues. Reactive Oxygen Species 249-252 angiotensinogen Homo sapiens 0-6 24587981-5 2012 In particular, the involvement of Ang II-induced ROS generation in arrhythmias, cell death/heart failure, ischemia/reperfusion injury, cardiac hypertrophy and hypertension are discussed. Reactive Oxygen Species 49-52 angiotensinogen Homo sapiens 34-40 22214405-2 2012 Angiotensin II (Ang II) is a major regulator of aldosterone synthesis and secretion, and it is known to facilitate reactive oxygen species (ROS) generation in many cell types. Reactive Oxygen Species 115-138 angiotensinogen Homo sapiens 0-14 22214405-2 2012 Angiotensin II (Ang II) is a major regulator of aldosterone synthesis and secretion, and it is known to facilitate reactive oxygen species (ROS) generation in many cell types. Reactive Oxygen Species 115-138 angiotensinogen Homo sapiens 16-22 22214405-2 2012 Angiotensin II (Ang II) is a major regulator of aldosterone synthesis and secretion, and it is known to facilitate reactive oxygen species (ROS) generation in many cell types. Reactive Oxygen Species 140-143 angiotensinogen Homo sapiens 0-14 22214405-2 2012 Angiotensin II (Ang II) is a major regulator of aldosterone synthesis and secretion, and it is known to facilitate reactive oxygen species (ROS) generation in many cell types. Reactive Oxygen Species 140-143 angiotensinogen Homo sapiens 16-22 22214405-3 2012 AIMS: Here, we assessed the role of ROS signaling in Ang II-induced aldosterone synthesis by focusing on the regulation of aldosterone synthase (CYP11B2), a cytochrome P450 oxidase that catalyzes the final step in aldosterone biosynthetic pathway. Reactive Oxygen Species 36-39 angiotensinogen Homo sapiens 53-59 22214405-4 2012 RESULTS: Ang II increased CYP11B2 activity, mRNA and protein with a concomitant elevation of 6-Carboxy- 2",7"-dichlorodihydrofluorescein diacetate fluorescence, malondialdehyde and protein carbonyl levels (indices of ROS), NADPH oxidase (Nox) activity, and H(2)O(2) levels in human and rat adrenal cortical cells. Reactive Oxygen Species 217-220 angiotensinogen Homo sapiens 9-15 23431467-7 2013 Another factor associated with insulin resistance in CKD is angiotensin II (Ang II) which appears to induce its intracellular effects through inflammatory cytokines or reactive oxygen species. Reactive Oxygen Species 168-191 angiotensinogen Homo sapiens 60-74 23431467-7 2013 Another factor associated with insulin resistance in CKD is angiotensin II (Ang II) which appears to induce its intracellular effects through inflammatory cytokines or reactive oxygen species. Reactive Oxygen Species 168-191 angiotensinogen Homo sapiens 76-82 22898098-4 2012 When iron is also present, CMPF and A-II induce the Fenton reaction, resulting in a further increase in ROS production. Reactive Oxygen Species 104-107 angiotensinogen Homo sapiens 36-40 22964022-4 2012 We previously demonstrated that myoblasts responded to Ang-II by increasing the ECM protein levels mediated by AT-1 receptors, implicating an Ang-II-induced reactive oxygen species (ROS) by a NAD(P)H oxidase-dependent mechanism. Reactive Oxygen Species 157-180 angiotensinogen Homo sapiens 142-148 22964022-4 2012 We previously demonstrated that myoblasts responded to Ang-II by increasing the ECM protein levels mediated by AT-1 receptors, implicating an Ang-II-induced reactive oxygen species (ROS) by a NAD(P)H oxidase-dependent mechanism. Reactive Oxygen Species 182-185 angiotensinogen Homo sapiens 142-148 22964022-9 2012 Furthermore, we showed that the Ang-II-dependent p38MAPK activation, but not the ERK1/2 phosphorylation, was necessary for the NOX-derived ROS. Reactive Oxygen Species 139-142 angiotensinogen Homo sapiens 32-38 22964022-11 2012 These results strongly suggest that the fibrotic response to Ang-II is mediated by the AT-1 receptor and requires the p38MAPK phosphorylation, NOX-induced ROS, and TGF-beta1 expression increase mediated by Ang-II in skeletal muscle cells. Reactive Oxygen Species 155-158 angiotensinogen Homo sapiens 61-67 22781707-11 2012 Taken together, these findings indicate that indoxyl sulfate enhances Ang II signaling through reactive oxygen species-induced EGFR expression. Reactive Oxygen Species 95-118 angiotensinogen Homo sapiens 70-76 22659808-0 2012 Rosiglitazone inhibits angiotensin II-induced C-reactive protein production in human aortic endothelial cells through regulating AT(1)-ROS-MAPK signal pathway. Reactive Oxygen Species 135-138 angiotensinogen Homo sapiens 23-37 22569796-6 2012 Meanwhile, choline pretreatment prevented the augment of reactive oxygen species (ROS) and intracellular calcium concentration in Ang II-treated cardiomyocytes. Reactive Oxygen Species 82-85 angiotensinogen Homo sapiens 130-136 22569796-8 2012 In conclusion, choline prevents Ang II-induced cardiac hypertrophy through inhibition of ROS-mediated p38 MAPK activation as well as regulation of Ca(2+)-mediated calcineurin signal transduction pathway. Reactive Oxygen Species 89-92 angiotensinogen Homo sapiens 32-38 22882945-4 2012 Multiple stimuli and agonists, such as transforming growth factor beta1, tumor necrosis factor, platelet derived growth factor, angiotensin II, hyperglycemia, oxidized low-density lipoprotein and albumin have been shown to alter the activity or expression of the NADPH oxidase and ultimately increase ROS production. Reactive Oxygen Species 301-304 angiotensinogen Homo sapiens 128-142 22519881-0 2012 Activation of PPARdelta counteracts angiotensin II-induced ROS generation by inhibiting rac1 translocation in vascular smooth muscle cells. Reactive Oxygen Species 59-62 angiotensinogen Homo sapiens 36-50 22215616-0 2012 Angiotensin II induces epithelial-to-mesenchymal transition in renal epithelial cells through reactive oxygen species/Src/caveolin-mediated activation of an epidermal growth factor receptor-extracellular signal-regulated kinase signaling pathway. Reactive Oxygen Species 94-117 angiotensinogen Homo sapiens 0-14 22919732-7 2012 Comparing with control group, Ang-II was able to increase [Ca2+]i and ROS level, decrease MMP level, inhibit complex IV activity and enhance caspase 3 activity in VECs, as a result, enhance apoptosis of VECs. Reactive Oxygen Species 70-73 angiotensinogen Homo sapiens 30-36 21861055-7 2011 Two or 6 h of Ang II (1 x 10(-7) mol/L) treatment caused an increase of ROS level in NRCFs, while this increase was inhibited with NaHS (1 x 10(-4) mol/L) treatment. Reactive Oxygen Species 72-75 angiotensinogen Homo sapiens 14-20 22318811-3 2012 Arterial stiffness is associated with the increased activity of angiotensin II, which results in increased NADPH oxidase activity, reduced NO bioavailability and increased production of reactive oxygen species. Reactive Oxygen Species 186-209 angiotensinogen Homo sapiens 64-78 22606238-7 2012 Exposure of cardiomyocytes to angiotensin II and norepinephrine led to ROS generation and M-CK carbonylation with loss of its enzymatic activity. Reactive Oxygen Species 71-74 angiotensinogen Homo sapiens 30-44 21755262-0 2011 Angiotensin-II-induced reactive oxygen species along the SFO-PVN-RVLM pathway: implications in neurogenic hypertension. Reactive Oxygen Species 23-46 angiotensinogen Homo sapiens 0-14 21755262-2 2011 This review is based on the premise that some forms of neurogenic hypertension are caused in part by the formation of angiotensin-II (Ang-II)-induced reactive oxygen species along the subfornical organ-paraventricular nucleus of the hypothalamus-rostral ventrolateral medulla pathway (SFO-PVN-RVLM pathway). Reactive Oxygen Species 150-173 angiotensinogen Homo sapiens 118-132 21755262-2 2011 This review is based on the premise that some forms of neurogenic hypertension are caused in part by the formation of angiotensin-II (Ang-II)-induced reactive oxygen species along the subfornical organ-paraventricular nucleus of the hypothalamus-rostral ventrolateral medulla pathway (SFO-PVN-RVLM pathway). Reactive Oxygen Species 150-173 angiotensinogen Homo sapiens 134-140 20626399-0 2012 Stimulation of reactive oxygen species and collagen synthesis by angiotensin II in cardiac fibroblasts. Reactive Oxygen Species 15-38 angiotensinogen Homo sapiens 65-79 20626399-3 2012 ANG II increases the NAD(P)H-dependent superoxide anion production and the intracellular generation of ROS in cardiac fibroblasts and apocynin, a membrane NAD(P)H oxidase inhibitor, abrogates this rise. Reactive Oxygen Species 103-106 angiotensinogen Homo sapiens 0-6 22101169-0 2012 Salvianolic acid A inhibits angiotensin II-induced proliferation of human umbilical vein endothelial cells by attenuating the production of ROS. Reactive Oxygen Species 140-143 angiotensinogen Homo sapiens 28-42 22101169-8 2012 Treatment of HUVECs with Ang II (1 mumol/L) dramatically increased ROS production in HUVECs; pretreatment of HUVECs with SalA (12.5, 25 and 50 mumol/L) blocked the ROS production in a concentration-dependent manner. Reactive Oxygen Species 67-70 angiotensinogen Homo sapiens 25-31 22101169-8 2012 Treatment of HUVECs with Ang II (1 mumol/L) dramatically increased ROS production in HUVECs; pretreatment of HUVECs with SalA (12.5, 25 and 50 mumol/L) blocked the ROS production in a concentration-dependent manner. Reactive Oxygen Species 164-167 angiotensinogen Homo sapiens 25-31 22101169-9 2012 CONCLUSION: SalA inhibits Ang II-induced proliferation of HUVECs via reducing the expression levels of phospho-Src and phospho-Akt (473), thereby attenuating the production of ROS. Reactive Oxygen Species 176-179 angiotensinogen Homo sapiens 26-32 23185428-6 2012 In human umbilical vein endothelial cells (HUVECs) and human pulmonary arterial endothelial cells (HPAECs), angiotensin II and oxLDL time- or concentration-dependently enhanced Kv1.5 protein expression in parallel with the production of intracellular ROS and endothelial cell injury. Reactive Oxygen Species 251-254 angiotensinogen Homo sapiens 108-122 23049937-13 2012 Furthermore, in vitro treatment with DM reduced angiotensin II-induced reactive oxygen species and NADPH oxidase activation in human aortic endothelial cells. Reactive Oxygen Species 71-94 angiotensinogen Homo sapiens 48-62 22427991-5 2012 Zinc mimics Ang II by increasing reactive oxygen species (ROS), activating NADPH oxidase activity and Akt, and by downregulating ZnT3 and ZnT10 and inducing senescence. Reactive Oxygen Species 33-56 angiotensinogen Homo sapiens 12-18 22427991-5 2012 Zinc mimics Ang II by increasing reactive oxygen species (ROS), activating NADPH oxidase activity and Akt, and by downregulating ZnT3 and ZnT10 and inducing senescence. Reactive Oxygen Species 58-61 angiotensinogen Homo sapiens 12-18 22427991-11 2012 These data demonstrate that zinc homeostasis dysfunction by decreased expression of ZnT3 or ZnT10 promotes senescence and that Ang II-induced senescence is a zinc and ROS-dependent process. Reactive Oxygen Species 167-170 angiotensinogen Homo sapiens 127-133 22427991-12 2012 Our studies suggest that zinc might also affect other ROS-dependent processes induced by Ang II, such as hypertrophy and migration of smooth muscle cells. Reactive Oxygen Species 54-57 angiotensinogen Homo sapiens 89-95 21660462-5 2011 Incubation with polyethylene glycol-CAT prevented the Ang II-induced effects on reactive oxygen species (ROS) generation and myofibroblast differentiation. Reactive Oxygen Species 80-103 angiotensinogen Homo sapiens 54-60 21660462-5 2011 Incubation with polyethylene glycol-CAT prevented the Ang II-induced effects on reactive oxygen species (ROS) generation and myofibroblast differentiation. Reactive Oxygen Species 105-108 angiotensinogen Homo sapiens 54-60 21930596-8 2011 Finally, this study suggests that the renin-angiotensin system may participate in the overproduction of reactive oxygen species associated with IH by upregulation of the actions of angiotensin II. Reactive Oxygen Species 104-127 angiotensinogen Homo sapiens 181-195 21947470-6 2011 Treatment of arteries of normal pregnant women with reactive oxygen species or activated neutrophils enhanced vessel reactivity to angiotensin II mimicking preeclamptic vessels. Reactive Oxygen Species 52-75 angiotensinogen Homo sapiens 131-145 22065936-6 2011 The adjuvant use of Trz can potentiate cardiomyocyte damage through a "dual-hit" mechanism, which includes inhibition of the neuregulin-1 survival signalling pathway and angiotensin II-induced activation of NADPH oxidase, with the ability to further increase reactive oxygen species production. Reactive Oxygen Species 259-282 angiotensinogen Homo sapiens 170-184 21257347-1 2011 Reactive oxygen species (ROS) are important intra-neuronal signaling intermediates in angiotensin II (AngII)-related neuro-cardiovascular diseases associated with excessive sympathoexcitation, including hypertension and heart failure. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 86-100 21693104-0 2011 Fibrotic response induced by angiotensin-II requires NAD(P)H oxidase-induced reactive oxygen species (ROS) in skeletal muscle cells. Reactive Oxygen Species 77-100 angiotensinogen Homo sapiens 29-43 21693104-0 2011 Fibrotic response induced by angiotensin-II requires NAD(P)H oxidase-induced reactive oxygen species (ROS) in skeletal muscle cells. Reactive Oxygen Species 102-105 angiotensinogen Homo sapiens 29-43 21693104-7 2011 Remarkably, Ang-II induced reactive oxygen species (ROS) via a NAD(P)H oxidase-dependent mechanism, as shown by inhibition of ROS production via the NAD(P)H oxidase inhibitors diphenylene iodonium (DPI) and apocynin. Reactive Oxygen Species 27-50 angiotensinogen Homo sapiens 12-18 21693104-7 2011 Remarkably, Ang-II induced reactive oxygen species (ROS) via a NAD(P)H oxidase-dependent mechanism, as shown by inhibition of ROS production via the NAD(P)H oxidase inhibitors diphenylene iodonium (DPI) and apocynin. Reactive Oxygen Species 52-55 angiotensinogen Homo sapiens 12-18 21693104-7 2011 Remarkably, Ang-II induced reactive oxygen species (ROS) via a NAD(P)H oxidase-dependent mechanism, as shown by inhibition of ROS production via the NAD(P)H oxidase inhibitors diphenylene iodonium (DPI) and apocynin. Reactive Oxygen Species 126-129 angiotensinogen Homo sapiens 12-18 21693104-8 2011 This increase in ROS is critical for Ang-II-induced fibrotic effects, as indicated by the decrease in Ang-II-induced CTGF and fibronectin levels by DPI and apocynin. Reactive Oxygen Species 17-20 angiotensinogen Homo sapiens 37-43 21693104-8 2011 This increase in ROS is critical for Ang-II-induced fibrotic effects, as indicated by the decrease in Ang-II-induced CTGF and fibronectin levels by DPI and apocynin. Reactive Oxygen Species 17-20 angiotensinogen Homo sapiens 102-108 21693104-9 2011 We also show that Ang-II-induced ROS production and fibrosis require PKC activity as indicated by the generic PKC inhibitor chelerythrine. Reactive Oxygen Species 33-36 angiotensinogen Homo sapiens 18-24 21693104-10 2011 These results strongly suggest that the fibrotic response induced by Ang-II is mediated by AT-1 receptor and requires NAD(P)H-induced ROS in skeletal muscle cells. Reactive Oxygen Species 134-137 angiotensinogen Homo sapiens 69-75 21436462-3 2011 Reactive oxygen species (ROS) produced by ANG II employ NADPH and xanthine oxidase pathways. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 42-48 21436462-3 2011 Reactive oxygen species (ROS) produced by ANG II employ NADPH and xanthine oxidase pathways. Reactive Oxygen Species 25-28 angiotensinogen Homo sapiens 42-48 21436462-15 2011 This suggests that ROS, produced by ANG II via NADPH and xanthine oxidase pathways, modulates the response of skin to the application of heat, and thus contributes to the control of local cutaneous blood flow. Reactive Oxygen Species 19-22 angiotensinogen Homo sapiens 36-42 21050133-2 2011 HGF has been shown to antagonize the angiotensin II-induced senescence of endothelial progenitor cells (EPCs), which is mediated by NADPH oxidase-dependent reactive oxygen species (ROS) formation. Reactive Oxygen Species 156-179 angiotensinogen Homo sapiens 37-51 21050133-2 2011 HGF has been shown to antagonize the angiotensin II-induced senescence of endothelial progenitor cells (EPCs), which is mediated by NADPH oxidase-dependent reactive oxygen species (ROS) formation. Reactive Oxygen Species 181-184 angiotensinogen Homo sapiens 37-51 21747283-3 2011 Ang II infusion induces skeletal muscle atrophy in rodents and mechanisms include increased expression of the E3 ligases atrogin-1/MuRF-1, an elevated rate of ubiquitin-proteasome mediated proteolysis and increased reactive oxygen species (ROS) levels, closely mimicking conditions of human cachexia. Reactive Oxygen Species 215-238 angiotensinogen Homo sapiens 0-6 21747283-3 2011 Ang II infusion induces skeletal muscle atrophy in rodents and mechanisms include increased expression of the E3 ligases atrogin-1/MuRF-1, an elevated rate of ubiquitin-proteasome mediated proteolysis and increased reactive oxygen species (ROS) levels, closely mimicking conditions of human cachexia. Reactive Oxygen Species 240-243 angiotensinogen Homo sapiens 0-6 21747283-5 2011 Nicotinamide adenine dinucleotide phosphate oxidase- and mitochondria-derived ROS contribute to ang II-induced oxidative stress. Reactive Oxygen Species 78-81 angiotensinogen Homo sapiens 96-102 21788998-0 2011 Angiotensin II-derived reactive oxygen species underpinning the processing of the cardiovascular reflexes in the medulla oblongata. Reactive Oxygen Species 23-46 angiotensinogen Homo sapiens 0-14 21788998-4 2011 It is well-known that one of the mechanisms by which angiotensin II exerts its effect is via the activation of pathways that generate reactive oxygen species (ROS). Reactive Oxygen Species 134-157 angiotensinogen Homo sapiens 53-67 21788998-4 2011 It is well-known that one of the mechanisms by which angiotensin II exerts its effect is via the activation of pathways that generate reactive oxygen species (ROS). Reactive Oxygen Species 159-162 angiotensinogen Homo sapiens 53-67 21257347-1 2011 Reactive oxygen species (ROS) are important intra-neuronal signaling intermediates in angiotensin II (AngII)-related neuro-cardiovascular diseases associated with excessive sympathoexcitation, including hypertension and heart failure. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 102-107 21257347-1 2011 Reactive oxygen species (ROS) are important intra-neuronal signaling intermediates in angiotensin II (AngII)-related neuro-cardiovascular diseases associated with excessive sympathoexcitation, including hypertension and heart failure. Reactive Oxygen Species 25-28 angiotensinogen Homo sapiens 86-100 21257347-1 2011 Reactive oxygen species (ROS) are important intra-neuronal signaling intermediates in angiotensin II (AngII)-related neuro-cardiovascular diseases associated with excessive sympathoexcitation, including hypertension and heart failure. Reactive Oxygen Species 25-28 angiotensinogen Homo sapiens 102-107 21257347-4 2011 This review focuses on recent studies that have revealed details on the AngII-activated sources of ROS, the downstream redox-sensitive effectors, Ang-(1-7)-stimulated increase in nitric oxide, and the neuro-cardiovascular (patho)physiological responses modulated by these reactive species. Reactive Oxygen Species 99-102 angiotensinogen Homo sapiens 72-77 21271181-8 2011 ANG II-induced MMP-9 expression was significantly reduced by 75 and 67%, respectively, by co-incubation of the cells with a selective inhibitor of protein kinase C (GF109203X, 5 microM) or of rho kinase (Y-27632, 15 microM), but not with inhibitors of phosphoinositide 3-kinase (wortmannin, 200 nM), tyrosine kinases (genistein, 100 microM) or of reactive oxygen species (alpha-tocopherol, 100 microM). Reactive Oxygen Species 347-370 angiotensinogen Homo sapiens 0-6 21270817-0 2011 Angiotensin II induces human astrocyte senescence through reactive oxygen species production. Reactive Oxygen Species 58-81 angiotensinogen Homo sapiens 0-14 21270817-2 2011 This study was conducted to determine the roles of reactive oxygen species production in Ang II-induced cellular senescence in cultured human astrocytes. Reactive Oxygen Species 51-74 angiotensinogen Homo sapiens 89-95 21228777-3 2011 The modulation of the vasomotor system involves ROS as mediators of vasoconstriction induced by angiotensin II, endothelin-1 and urotensin-II, among others. Reactive Oxygen Species 48-51 angiotensinogen Homo sapiens 96-110 20971763-8 2011 ANG II (600 ng kg(-1) min(-1)) augmented neocortical reactive oxygen species (ROS) with a time course similar to that of the cerebrovascular dysfunction. Reactive Oxygen Species 57-80 angiotensinogen Homo sapiens 0-6 21317849-3 2011 Recent evidences suggest that the major source of ROS is the NADPH-oxidase, especially activated by angiotensin II, shear stress and hyperglycemia. Reactive Oxygen Species 50-53 angiotensinogen Homo sapiens 100-114 21093722-3 2011 Angiotensin II (Ang II) promotes inflammation and the generation of reactive oxygen species and governs onset and progression of vascular senescence, which are all associated with functional and structural changes, contributing to age-related diseases. Reactive Oxygen Species 68-91 angiotensinogen Homo sapiens 0-14 21093722-3 2011 Angiotensin II (Ang II) promotes inflammation and the generation of reactive oxygen species and governs onset and progression of vascular senescence, which are all associated with functional and structural changes, contributing to age-related diseases. Reactive Oxygen Species 68-91 angiotensinogen Homo sapiens 16-22 20971763-8 2011 ANG II (600 ng kg(-1) min(-1)) augmented neocortical reactive oxygen species (ROS) with a time course similar to that of the cerebrovascular dysfunction. Reactive Oxygen Species 82-85 angiotensinogen Homo sapiens 0-6 20819950-2 2011 Angiotensin II (Ang II) enhances ROS production by activating NAD(P)H oxidase and uncoupling endothelial nitric oxide synthase (NOS). Reactive Oxygen Species 33-36 angiotensinogen Homo sapiens 0-14 20819950-2 2011 Angiotensin II (Ang II) enhances ROS production by activating NAD(P)H oxidase and uncoupling endothelial nitric oxide synthase (NOS). Reactive Oxygen Species 33-36 angiotensinogen Homo sapiens 16-22 21841319-13 2011 CONCLUSION: Ang II accelerates late EPCs senescence mainly via increased ROS originating from NOX2 and NOX4 up-regulation or translocated NOX5. Reactive Oxygen Species 73-76 angiotensinogen Homo sapiens 12-18 21325823-7 2011 Losartan and complex II inhibitor TIFA decreased Ang II -stimulated reactive oxygen species (ROS) generation, and antioxidant NAC completely abolished Ang II -induced CRP expression in U937 macrophages. Reactive Oxygen Species 68-91 angiotensinogen Homo sapiens 49-55 21325823-7 2011 Losartan and complex II inhibitor TIFA decreased Ang II -stimulated reactive oxygen species (ROS) generation, and antioxidant NAC completely abolished Ang II -induced CRP expression in U937 macrophages. Reactive Oxygen Species 93-96 angiotensinogen Homo sapiens 49-55 21325823-9 2011 These demonstrate that Ang II is capable of inducing CRP generation in macrophages via AT(1)-ROS-ERK1/2/p38MAPK-NF-kappaB signal pathway, which contributes to better understanding of the proinflammatory and proatherosclerotic actions of Ang II. Reactive Oxygen Species 93-96 angiotensinogen Homo sapiens 23-29 21067505-5 2011 Additionally, angiotensin II promotes podocyte injury indirectly by increasing calcium influx and production of reactive oxygen species. Reactive Oxygen Species 112-135 angiotensinogen Homo sapiens 14-28 21747985-6 2011 In the present paper, major angiotensin II-induced vascular ROS generation within the vasculature, and relative sources, will be discussed. Reactive Oxygen Species 60-63 angiotensinogen Homo sapiens 28-42 21747985-7 2011 Recent development of signalling pathways whereby angiotensin II-driven vascular ROS induce and accelerate functional and structural vascular injury will be also considered. Reactive Oxygen Species 81-84 angiotensinogen Homo sapiens 50-64 20978160-0 2010 Cis-dichlorodiammineplatinum upregulates angiotensin II type 1 receptors through reactive oxygen species generation and enhances VEGF production in bladder cancer. Reactive Oxygen Species 81-104 angiotensinogen Homo sapiens 41-55 20832068-7 2010 Exogenous application of CGRP inhibited Ang II-induced EPCs senescence by down-regulating the expression of NADPH oxidase and reactive oxygen species production. Reactive Oxygen Species 126-149 angiotensinogen Homo sapiens 40-46 20832068-11 2010 CONCLUSIONS: The results suggest that CGRP can counteract Ang II-induced EPCs senescence through down-regulating the expression of NADPH oxidase and reactive oxygen species production and increasing the production of klotho. Reactive Oxygen Species 149-172 angiotensinogen Homo sapiens 58-64 20692267-3 2010 We have recently reported that angiotensin II (Ang II) stimulated total NBC activity during the recovery from intracellular acidosis through a reactive oxygen species (ROS) and ERK-dependent pathway. Reactive Oxygen Species 143-166 angiotensinogen Homo sapiens 31-45 20692267-3 2010 We have recently reported that angiotensin II (Ang II) stimulated total NBC activity during the recovery from intracellular acidosis through a reactive oxygen species (ROS) and ERK-dependent pathway. Reactive Oxygen Species 168-171 angiotensinogen Homo sapiens 31-45 21051828-12 2010 Ghrelin decreased the reactive oxygen species in HUVECs induced by Ang II. Reactive Oxygen Species 22-45 angiotensinogen Homo sapiens 67-73 20798361-8 2010 CONCLUSIONS: Our data support a novel model of local oxidative regulation of Ca(2+) influx where vasoconstrictors coupled to NAPDH oxidase (eg, angiotensin II) induce discrete sites of ROS generation resulting in oxidative activation of adjacent protein kinase Calpha molecules that in turn promote local sites of enhanced L-type Ca(2+) channel activity, resulting in increased Ca(2+) influx and contraction. Reactive Oxygen Species 185-188 angiotensinogen Homo sapiens 144-158 20660157-10 2010 Furthermore, inhibition of mitochondrial-generated ROS abolished HIF-1alpha protein stability, HIF-1-dependent transcription and VSMC migration by Ang II. Reactive Oxygen Species 51-54 angiotensinogen Homo sapiens 147-153 20660157-11 2010 A large number of studies implicate NADPH oxidase-generated ROS in Ang II-mediated signaling pathways in VSMCs. Reactive Oxygen Species 60-63 angiotensinogen Homo sapiens 67-73 20660157-5 2010 Additionally, the generation of reactive oxygen species (ROS) is essential for HIF-1 activation during Ang II treatment. Reactive Oxygen Species 32-55 angiotensinogen Homo sapiens 103-109 20660157-5 2010 Additionally, the generation of reactive oxygen species (ROS) is essential for HIF-1 activation during Ang II treatment. Reactive Oxygen Species 57-60 angiotensinogen Homo sapiens 103-109 20538278-10 2010 Losartan and TIFA decreased AngII-stimulated ROS generation, and antioxidant NAC completely abolished AngII-induced CRP expression in HAECs. Reactive Oxygen Species 45-48 angiotensinogen Homo sapiens 28-33 20538278-12 2010 CONCLUSIONS: The present study demonstrates that AngII has ability to induce CRP expression in HAECs through AT(1)-ROS-ERK1/2 and JNK-NF-kappaB signal pathway, which strengthens understanding of the proinflammatory and proathroscerotic actions of AngII. Reactive Oxygen Species 115-118 angiotensinogen Homo sapiens 49-54 20696982-10 2010 Thus, angiotensin II increased cellular asymmetrical dimethylarginine via type 1 receptors and reactive oxygen species. Reactive Oxygen Species 95-118 angiotensinogen Homo sapiens 6-20 20122895-3 2010 In the first model, angiotensin-II is discussed as a trigger for NADPH oxidase activation with subsequent ROS-dependent opening of mitochondrial ATP-sensitive potassium channels leading to depolarization of mitochondrial membrane potential followed by mitochondrial ROS formation and respiratory dysfunction. Reactive Oxygen Species 106-109 angiotensinogen Homo sapiens 20-34 20431588-1 2010 Angiotensin II (Ang II)-induced endothelial injury, which is associated with atherosclerosis, is believed to be mediated by intracellular reactive oxygen species (ROS) through stimulation of nicotinamide adenine dinucleotide phosphate oxidase (NOX). Reactive Oxygen Species 138-161 angiotensinogen Homo sapiens 0-22 20431588-1 2010 Angiotensin II (Ang II)-induced endothelial injury, which is associated with atherosclerosis, is believed to be mediated by intracellular reactive oxygen species (ROS) through stimulation of nicotinamide adenine dinucleotide phosphate oxidase (NOX). Reactive Oxygen Species 163-166 angiotensinogen Homo sapiens 0-22 20122895-3 2010 In the first model, angiotensin-II is discussed as a trigger for NADPH oxidase activation with subsequent ROS-dependent opening of mitochondrial ATP-sensitive potassium channels leading to depolarization of mitochondrial membrane potential followed by mitochondrial ROS formation and respiratory dysfunction. Reactive Oxygen Species 266-269 angiotensinogen Homo sapiens 20-34 20086047-7 2010 Moreover, MEF2 activation via reactive oxygen species and p38 mitogen-activated protein kinase induced KLF5 expression in response to AII, and KLF5 and MEF2 were coexpressed in coronary atherosclerotic plaques. Reactive Oxygen Species 30-53 angiotensinogen Homo sapiens 134-137 19485896-3 2010 The metabolic abnormalities associated with diabetes lead to activation of the renin-angiotensin-aldosterone system (RAAS), with a subsequent increase of angiotensin II and aldosterone levels, which might alter the insulin signaling pathway and promote the formation of reactive oxygen species that induce endothelial dysfunction as well as cardiovascular disease and renal disease. Reactive Oxygen Species 270-293 angiotensinogen Homo sapiens 154-168 20384568-0 2010 Direct inhibition by angiotensin II of insulin-dependent glucose transport activity in mammalian skeletal muscle involves a ROS-dependent mechanism. Reactive Oxygen Species 124-127 angiotensinogen Homo sapiens 21-35 19940161-2 2010 Reactive oxygen species (ROS) are important mediators of Ang II-induced signaling generally and have a well defined role in vascular hypertrophy, which is inhibited by overexpression of catalase, inferring a specific role of H(2)O(2). Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 57-63 20299739-4 2010 Many of these atherogenic actions of Ang II are mediated by reactive oxygen species (ROS). Reactive Oxygen Species 60-83 angiotensinogen Homo sapiens 37-43 20299739-4 2010 Many of these atherogenic actions of Ang II are mediated by reactive oxygen species (ROS). Reactive Oxygen Species 85-88 angiotensinogen Homo sapiens 37-43 19940161-10 2010 We provide novel mechanistic insights by which Ang II may mediate its ROS-dependent pathophysiologic effects on multiple cardiometabolic diseases. Reactive Oxygen Species 70-73 angiotensinogen Homo sapiens 47-53 19940161-2 2010 Reactive oxygen species (ROS) are important mediators of Ang II-induced signaling generally and have a well defined role in vascular hypertrophy, which is inhibited by overexpression of catalase, inferring a specific role of H(2)O(2). Reactive Oxygen Species 25-28 angiotensinogen Homo sapiens 57-63 19781192-0 2009 [NADPH oxidase-derived reactive oxygen species involved in angiotensin II-induced monocyte chemoattractant protein-1 expression in mesangial cells]. Reactive Oxygen Species 23-46 angiotensinogen Homo sapiens 59-73 19864304-7 2010 ANG II also induced ROS from NADPH oxidase. Reactive Oxygen Species 20-23 angiotensinogen Homo sapiens 0-6 19864304-8 2010 High glucose and ANG II upregulated (100%) COX-2 via ROS and significantly increased the synthesis of prostacyclin (PGI(2)) by 300%. Reactive Oxygen Species 53-56 angiotensinogen Homo sapiens 17-23 19864304-10 2010 These novel studies are the first in human GEC that characterize the differential role of FFA, hyperglycemia, and ANG II on the genesis of ROS, COX-2, and PGs and their interplay in the early stages of hyperglcyemia. Reactive Oxygen Species 139-142 angiotensinogen Homo sapiens 114-120 19652871-7 2009 Moreover, the formation of reactive oxygen species generated by vascular enzyme systems may play a critical role in the regulation of IL-6 indicating a cross talk between vasoactive substances i.e. angiotensin II or adrenalin and pro-inflammatory cytokines such as IL-6. Reactive Oxygen Species 27-50 angiotensinogen Homo sapiens 198-212 19328808-4 2009 MIP-1beta or AngII stimulation significantly increased ROS production and adhesion of THP-1 cells to inflamed human umbilical vein endothelial cells. Reactive Oxygen Species 55-58 angiotensinogen Homo sapiens 13-18 19328808-7 2009 Moreover, cell adhesion and ROS production stimulated with MIP-1beta or AngII were completely inhibited by fluvastatin. Reactive Oxygen Species 28-31 angiotensinogen Homo sapiens 72-77 19646989-0 2009 Role of reactive oxygen species (ROS) in angiotensin II-induced stimulation of the cardiac Na+/HCO3- cotransport. Reactive Oxygen Species 8-31 angiotensinogen Homo sapiens 41-55 19646989-0 2009 Role of reactive oxygen species (ROS) in angiotensin II-induced stimulation of the cardiac Na+/HCO3- cotransport. Reactive Oxygen Species 33-36 angiotensinogen Homo sapiens 41-55 19646989-8 2009 We also determined the phosphorylation of ERK during the first min of acidosis and we detected that Ang II significantly enhanced the ERK phosphorylation levels, an effect that was cancelled by scavenging ROS with MPG. Reactive Oxygen Species 205-208 angiotensinogen Homo sapiens 100-106 19646989-9 2009 In conclusion, we propose that Ang II enhances the production of ROS through the activation of the NADPH oxidase, which in turn triggers mK(ATP) opening and mitochondrial ROS production ("ROS-induced ROS-release mechanism"). Reactive Oxygen Species 65-68 angiotensinogen Homo sapiens 31-37 19646989-9 2009 In conclusion, we propose that Ang II enhances the production of ROS through the activation of the NADPH oxidase, which in turn triggers mK(ATP) opening and mitochondrial ROS production ("ROS-induced ROS-release mechanism"). Reactive Oxygen Species 171-174 angiotensinogen Homo sapiens 31-37 19646989-9 2009 In conclusion, we propose that Ang II enhances the production of ROS through the activation of the NADPH oxidase, which in turn triggers mK(ATP) opening and mitochondrial ROS production ("ROS-induced ROS-release mechanism"). Reactive Oxygen Species 171-174 angiotensinogen Homo sapiens 31-37 19646989-9 2009 In conclusion, we propose that Ang II enhances the production of ROS through the activation of the NADPH oxidase, which in turn triggers mK(ATP) opening and mitochondrial ROS production ("ROS-induced ROS-release mechanism"). Reactive Oxygen Species 171-174 angiotensinogen Homo sapiens 31-37 19781192-1 2009 OBJECTIVE: To investigate the origin of oxidative stress induced by angiotensin II (AngII) in human mesangial cells and the role of reactive oxygen species (ROS) in AngII-induced monocyte chemoattractant protein-1 (MCP-1) expression. Reactive Oxygen Species 132-155 angiotensinogen Homo sapiens 165-170 19781192-1 2009 OBJECTIVE: To investigate the origin of oxidative stress induced by angiotensin II (AngII) in human mesangial cells and the role of reactive oxygen species (ROS) in AngII-induced monocyte chemoattractant protein-1 (MCP-1) expression. Reactive Oxygen Species 157-160 angiotensinogen Homo sapiens 165-170 19781192-10 2009 AngII increased intracellular ROS production as early as 3 min with the peak at 60 min and was in a time and dose-dependent. Reactive Oxygen Species 30-33 angiotensinogen Homo sapiens 0-5 19781192-11 2009 Incubation with different dosages of AngII (1 nmol/L, 10 nmol/L, and 100 nmol/L AngII) for 60 min, ROS production increased at 1.82, 2.92, and 4.08 folds respectively. Reactive Oxygen Species 99-102 angiotensinogen Homo sapiens 37-42 19781192-11 2009 Incubation with different dosages of AngII (1 nmol/L, 10 nmol/L, and 100 nmol/L AngII) for 60 min, ROS production increased at 1.82, 2.92, and 4.08 folds respectively. Reactive Oxygen Species 99-102 angiotensinogen Homo sapiens 80-85 19781192-12 2009 AngII-induced ROS generation was sensitive to diphenyleneiodonium sulfate (DPI, 10 micromol/L) and apocynin (500 micromol/L), two structurally distinct NADPH oxidase inhibitors. Reactive Oxygen Species 14-17 angiotensinogen Homo sapiens 0-5 19781192-14 2009 AngII-induced ROS generation was inhibited by the AT1 antagonist losartan (10 micromol/L) but not the AT2 antagonist PD123319 (10 micromol/L). Reactive Oxygen Species 14-17 angiotensinogen Homo sapiens 0-5 19781192-18 2009 CONCLUSIONS: NADPH oxidase-derived ROS is involved in AngII-induced MCP-1 expression. Reactive Oxygen Species 35-38 angiotensinogen Homo sapiens 54-59 19339277-6 2009 Similarly, the formation of endogenous ROS stimulated by angiotensin II (AngII) also activates the SSH-1L-cofilin pathway via oxidation of 14-3-3zeta to increase AngII-induced membrane ruffling and cell motility. Reactive Oxygen Species 39-42 angiotensinogen Homo sapiens 57-71 19339277-6 2009 Similarly, the formation of endogenous ROS stimulated by angiotensin II (AngII) also activates the SSH-1L-cofilin pathway via oxidation of 14-3-3zeta to increase AngII-induced membrane ruffling and cell motility. Reactive Oxygen Species 39-42 angiotensinogen Homo sapiens 73-78 19339277-6 2009 Similarly, the formation of endogenous ROS stimulated by angiotensin II (AngII) also activates the SSH-1L-cofilin pathway via oxidation of 14-3-3zeta to increase AngII-induced membrane ruffling and cell motility. Reactive Oxygen Species 39-42 angiotensinogen Homo sapiens 162-167 19059306-1 2009 Over the last decade many studies have demonstrated the importance of reactive oxygen species (ROS) production by NADPH oxidases in angiotensin II (Ang II) signaling, as well as a role for ROS in the development of different diseases in which Ang II is a central component. Reactive Oxygen Species 95-98 angiotensinogen Homo sapiens 148-154 19059306-1 2009 Over the last decade many studies have demonstrated the importance of reactive oxygen species (ROS) production by NADPH oxidases in angiotensin II (Ang II) signaling, as well as a role for ROS in the development of different diseases in which Ang II is a central component. Reactive Oxygen Species 95-98 angiotensinogen Homo sapiens 243-249 19059306-1 2009 Over the last decade many studies have demonstrated the importance of reactive oxygen species (ROS) production by NADPH oxidases in angiotensin II (Ang II) signaling, as well as a role for ROS in the development of different diseases in which Ang II is a central component. Reactive Oxygen Species 70-93 angiotensinogen Homo sapiens 132-146 19059306-1 2009 Over the last decade many studies have demonstrated the importance of reactive oxygen species (ROS) production by NADPH oxidases in angiotensin II (Ang II) signaling, as well as a role for ROS in the development of different diseases in which Ang II is a central component. Reactive Oxygen Species 70-93 angiotensinogen Homo sapiens 148-154 19059306-1 2009 Over the last decade many studies have demonstrated the importance of reactive oxygen species (ROS) production by NADPH oxidases in angiotensin II (Ang II) signaling, as well as a role for ROS in the development of different diseases in which Ang II is a central component. Reactive Oxygen Species 189-192 angiotensinogen Homo sapiens 243-249 19059306-1 2009 Over the last decade many studies have demonstrated the importance of reactive oxygen species (ROS) production by NADPH oxidases in angiotensin II (Ang II) signaling, as well as a role for ROS in the development of different diseases in which Ang II is a central component. Reactive Oxygen Species 95-98 angiotensinogen Homo sapiens 132-146 19059306-2 2009 In this review, we summarize the mechanism of activation of NADPH oxidases by Ang II and describe the molecular targets of ROS in Ang II signaling in the vasculature, kidney and brain. Reactive Oxygen Species 123-126 angiotensinogen Homo sapiens 130-136 18785879-8 2009 We conclude that AngII stimulation of vascular cells leads to a ROS-dependent increase in CD40/CD40L signalling pathway activity. Reactive Oxygen Species 64-67 angiotensinogen Homo sapiens 17-22 19348231-3 2009 In endothelial cells, AII, the key effector of the renin-angiotensin system (RAS), stimulates the production of reactive oxygen species (ROS) and negatively regulates the NO signaling pathway and thereby induces endothelial dysfunction. Reactive Oxygen Species 112-135 angiotensinogen Homo sapiens 22-25 19348231-3 2009 In endothelial cells, AII, the key effector of the renin-angiotensin system (RAS), stimulates the production of reactive oxygen species (ROS) and negatively regulates the NO signaling pathway and thereby induces endothelial dysfunction. Reactive Oxygen Species 137-140 angiotensinogen Homo sapiens 22-25 19348232-4 2009 Many of these atherogenic actions of Ang II are mediated by reactive oxygen species (ROS). Reactive Oxygen Species 60-83 angiotensinogen Homo sapiens 37-43 19348232-4 2009 Many of these atherogenic actions of Ang II are mediated by reactive oxygen species (ROS). Reactive Oxygen Species 85-88 angiotensinogen Homo sapiens 37-43 19138171-8 2009 Importantly, angiotensin II can either stimulate endothelial progenitor cells by improvement of vascular endothelial growth factor signalling, or invoke excessive production of reactive oxygen species causing premature senescence of these cells. Reactive Oxygen Species 177-200 angiotensinogen Homo sapiens 13-27 19417726-3 2009 It has been clinically demonstrated that the immunoreactivities of intrarenal heme oxygenase-1 (HO-1) and 4-hydroxy-2-nonenal (4-HNE) markers of reactive oxygen species (ROS) and those of intrarenal angiotensinogen (AGT) and angiotensin II (Ang II) markers of renin angiotensin system (RAS) in IgA nephropathy patients were significantly increased as compared to those of control subjects. Reactive Oxygen Species 145-168 angiotensinogen Homo sapiens 199-214 19417726-3 2009 It has been clinically demonstrated that the immunoreactivities of intrarenal heme oxygenase-1 (HO-1) and 4-hydroxy-2-nonenal (4-HNE) markers of reactive oxygen species (ROS) and those of intrarenal angiotensinogen (AGT) and angiotensin II (Ang II) markers of renin angiotensin system (RAS) in IgA nephropathy patients were significantly increased as compared to those of control subjects. Reactive Oxygen Species 145-168 angiotensinogen Homo sapiens 216-219 19417726-3 2009 It has been clinically demonstrated that the immunoreactivities of intrarenal heme oxygenase-1 (HO-1) and 4-hydroxy-2-nonenal (4-HNE) markers of reactive oxygen species (ROS) and those of intrarenal angiotensinogen (AGT) and angiotensin II (Ang II) markers of renin angiotensin system (RAS) in IgA nephropathy patients were significantly increased as compared to those of control subjects. Reactive Oxygen Species 145-168 angiotensinogen Homo sapiens 225-239 19417726-3 2009 It has been clinically demonstrated that the immunoreactivities of intrarenal heme oxygenase-1 (HO-1) and 4-hydroxy-2-nonenal (4-HNE) markers of reactive oxygen species (ROS) and those of intrarenal angiotensinogen (AGT) and angiotensin II (Ang II) markers of renin angiotensin system (RAS) in IgA nephropathy patients were significantly increased as compared to those of control subjects. Reactive Oxygen Species 145-168 angiotensinogen Homo sapiens 241-247 19417726-3 2009 It has been clinically demonstrated that the immunoreactivities of intrarenal heme oxygenase-1 (HO-1) and 4-hydroxy-2-nonenal (4-HNE) markers of reactive oxygen species (ROS) and those of intrarenal angiotensinogen (AGT) and angiotensin II (Ang II) markers of renin angiotensin system (RAS) in IgA nephropathy patients were significantly increased as compared to those of control subjects. Reactive Oxygen Species 170-173 angiotensinogen Homo sapiens 199-214 19417726-3 2009 It has been clinically demonstrated that the immunoreactivities of intrarenal heme oxygenase-1 (HO-1) and 4-hydroxy-2-nonenal (4-HNE) markers of reactive oxygen species (ROS) and those of intrarenal angiotensinogen (AGT) and angiotensin II (Ang II) markers of renin angiotensin system (RAS) in IgA nephropathy patients were significantly increased as compared to those of control subjects. Reactive Oxygen Species 170-173 angiotensinogen Homo sapiens 216-219 19417726-3 2009 It has been clinically demonstrated that the immunoreactivities of intrarenal heme oxygenase-1 (HO-1) and 4-hydroxy-2-nonenal (4-HNE) markers of reactive oxygen species (ROS) and those of intrarenal angiotensinogen (AGT) and angiotensin II (Ang II) markers of renin angiotensin system (RAS) in IgA nephropathy patients were significantly increased as compared to those of control subjects. Reactive Oxygen Species 170-173 angiotensinogen Homo sapiens 225-239 19417726-3 2009 It has been clinically demonstrated that the immunoreactivities of intrarenal heme oxygenase-1 (HO-1) and 4-hydroxy-2-nonenal (4-HNE) markers of reactive oxygen species (ROS) and those of intrarenal angiotensinogen (AGT) and angiotensin II (Ang II) markers of renin angiotensin system (RAS) in IgA nephropathy patients were significantly increased as compared to those of control subjects. Reactive Oxygen Species 170-173 angiotensinogen Homo sapiens 241-247 18756259-5 2008 DETC also reduced the intracellular generation of reactive oxygen species (ROS) (such as H2O2, hydroxyl radicals, hydroperoxides) in control and ANG II-treated fibroblasts, whereas tempol reduced the ROS production only in ANG II-treated fibroblasts. Reactive Oxygen Species 75-78 angiotensinogen Homo sapiens 145-151 18845352-8 2008 Intensive glycemic control and inhibition of angiotensin II delay the onset and progression of diabetic nephropathy, in part, through prevention of overproduction of ROS. Reactive Oxygen Species 166-169 angiotensinogen Homo sapiens 45-59 18424077-0 2008 Angiotensin II enhances EGF receptor expression levels via ROS formation in HaCaT cells. Reactive Oxygen Species 59-62 angiotensinogen Homo sapiens 0-14 18855718-6 2008 Angiotensin II acting through the AT1 receptor can inhibit insulin-induced nitric oxide (NO) production by activating ERK 1/2 and JNK and enhances the activity of NADPH oxidase that leads to an increased reactive oxygen species generation. Reactive Oxygen Species 204-227 angiotensinogen Homo sapiens 0-14 18424077-1 2008 BACKGROUND: Recent work has shown a novel function of angiotensin II (Ang II) in skin wound healing in which reactive oxygen species might be involved. Reactive Oxygen Species 109-132 angiotensinogen Homo sapiens 54-68 18424077-1 2008 BACKGROUND: Recent work has shown a novel function of angiotensin II (Ang II) in skin wound healing in which reactive oxygen species might be involved. Reactive Oxygen Species 109-132 angiotensinogen Homo sapiens 70-76 18559349-6 2008 Ang II also up-regulates Nox4 protein, and siNox4 abrogates the Ang II-induced increase in intracellular reactive oxygen species (ROS) generation. Reactive Oxygen Species 105-128 angiotensinogen Homo sapiens 0-6 18559349-9 2008 This work provides the first evidence that Nox4-derived ROS are responsible for Ang II-induced PDK-1 tyrosine phosphorylation and activation through stimulation of Src. Reactive Oxygen Species 56-59 angiotensinogen Homo sapiens 80-86 18779176-7 2008 Among the 3 siRNAs, siRNA-1 was the most powerful on gene silence with 50 nmol/L transfection concentration at 24 h and 36 h. The number of positive cells stained by beta-gal were increased in ECV-304 stimulated with Ang II, and p22phox mRNA and protein expression were increased in aging ECV-304 stimulated with Ang II, which had lower NO and higher ROS. Reactive Oxygen Species 351-354 angiotensinogen Homo sapiens 217-223 18779176-9 2008 The result of the present study suggested that siRNA could induce NAD(P)H oxidase subunit p22phox gene silence, Ang II could induce ECV-304 aging cultured in vitro, and the possible pathway of endothelial cell aging is that Ang II upregulates p22phox expression, and then enhances the cell ROS level. Reactive Oxygen Species 290-293 angiotensinogen Homo sapiens 112-118 18779176-9 2008 The result of the present study suggested that siRNA could induce NAD(P)H oxidase subunit p22phox gene silence, Ang II could induce ECV-304 aging cultured in vitro, and the possible pathway of endothelial cell aging is that Ang II upregulates p22phox expression, and then enhances the cell ROS level. Reactive Oxygen Species 290-293 angiotensinogen Homo sapiens 224-230 18559349-6 2008 Ang II also up-regulates Nox4 protein, and siNox4 abrogates the Ang II-induced increase in intracellular reactive oxygen species (ROS) generation. Reactive Oxygen Species 105-128 angiotensinogen Homo sapiens 64-70 18559349-6 2008 Ang II also up-regulates Nox4 protein, and siNox4 abrogates the Ang II-induced increase in intracellular reactive oxygen species (ROS) generation. Reactive Oxygen Species 130-133 angiotensinogen Homo sapiens 0-6 18559349-6 2008 Ang II also up-regulates Nox4 protein, and siNox4 abrogates the Ang II-induced increase in intracellular reactive oxygen species (ROS) generation. Reactive Oxygen Species 130-133 angiotensinogen Homo sapiens 64-70 18625248-1 2008 We have previously demonstrated the participation of reactive oxygen species (ROS) in the positive inotropic effect of a physiological concentration of Angiotensin II (Ang II, 1 nM). Reactive Oxygen Species 53-76 angiotensinogen Homo sapiens 152-166 18625248-1 2008 We have previously demonstrated the participation of reactive oxygen species (ROS) in the positive inotropic effect of a physiological concentration of Angiotensin II (Ang II, 1 nM). Reactive Oxygen Species 78-81 angiotensinogen Homo sapiens 152-166 18568954-7 2008 Dihydroethidium method showed that ox-LDL and angiotensin II increased the generation of intracellular ROS. Reactive Oxygen Species 103-106 angiotensinogen Homo sapiens 46-60 18515325-1 2008 Angiotensin II (Ang II) is a peptide hormone able to elicit a strong production of reactive oxygen species by human neutrophils. Reactive Oxygen Species 83-106 angiotensinogen Homo sapiens 0-14 18515325-1 2008 Angiotensin II (Ang II) is a peptide hormone able to elicit a strong production of reactive oxygen species by human neutrophils. Reactive Oxygen Species 83-106 angiotensinogen Homo sapiens 16-22 18373437-9 2008 Loss-of-function experiments indicate that PDI supports angiotensin II-mediated ROS generation and Akt phosphorylation. Reactive Oxygen Species 80-83 angiotensinogen Homo sapiens 56-70 18568954-8 2008 Once the expression of p22(phox) or NOXA1 was suppressed by siRNA, the generation of ROS induced by ox-LDL and angiotensin II were potently decreased. Reactive Oxygen Species 85-88 angiotensinogen Homo sapiens 111-125 17941088-0 2008 All-trans retinoic acid prevents angiotensin II- and mechanical stretch-induced reactive oxygen species generation and cardiomyocyte apoptosis. Reactive Oxygen Species 80-103 angiotensinogen Homo sapiens 33-47 18390537-6 2008 In a subgroup of patients, a reduced angiotensin II-induced ROS generation was also observed upon clinical simvastatin treatment. Reactive Oxygen Species 60-63 angiotensinogen Homo sapiens 37-51 18256310-1 2008 Reactive oxygen species (ROS) play important roles in renal vasoconstrictor responses to acute and chronic stimulation by angiotensin II and norepinephrine, as well as in long-term effects of endothelin-1 (ET-1). Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 122-136 18256310-1 2008 Reactive oxygen species (ROS) play important roles in renal vasoconstrictor responses to acute and chronic stimulation by angiotensin II and norepinephrine, as well as in long-term effects of endothelin-1 (ET-1). Reactive Oxygen Species 25-28 angiotensinogen Homo sapiens 122-136 17941088-6 2008 RA inhibited stretch- and Ang II-induced intracellular reactive oxygen species (ROS) generation and upregulated the SOD2 level. Reactive Oxygen Species 55-78 angiotensinogen Homo sapiens 26-32 17941088-6 2008 RA inhibited stretch- and Ang II-induced intracellular reactive oxygen species (ROS) generation and upregulated the SOD2 level. Reactive Oxygen Species 80-83 angiotensinogen Homo sapiens 26-32 17941088-10 2008 We also observed that both RAR and RXR were involved in preventing Ang II- and stretch-induced ROS production and apoptosis, by using selective retinoid receptor agonists and antagonists. Reactive Oxygen Species 95-98 angiotensinogen Homo sapiens 67-73 18287880-10 2008 p47 negatively regulates ROS generation under basal conditions, whereas it enhances AngII increased ROS production. Reactive Oxygen Species 100-103 angiotensinogen Homo sapiens 84-89 18365690-0 2008 Inhibitory effect of simvastatin on the TNF-alpha- and angiotensin II-induced monocyte adhesion to endothelial cells is mediated through the suppression of geranylgeranyl isoprenoid-dependent ROS generation. Reactive Oxygen Species 192-195 angiotensinogen Homo sapiens 55-69 17991883-1 2008 Angiotensin II (Ang II) induces reactive oxygen species (ROS) production by human vascular smooth muscle cells (hVSMCs). Reactive Oxygen Species 32-55 angiotensinogen Homo sapiens 0-14 17991883-1 2008 Angiotensin II (Ang II) induces reactive oxygen species (ROS) production by human vascular smooth muscle cells (hVSMCs). Reactive Oxygen Species 32-55 angiotensinogen Homo sapiens 16-22 17991883-1 2008 Angiotensin II (Ang II) induces reactive oxygen species (ROS) production by human vascular smooth muscle cells (hVSMCs). Reactive Oxygen Species 57-60 angiotensinogen Homo sapiens 0-14 17991883-1 2008 Angiotensin II (Ang II) induces reactive oxygen species (ROS) production by human vascular smooth muscle cells (hVSMCs). Reactive Oxygen Species 57-60 angiotensinogen Homo sapiens 16-22 17991883-4 2008 This study tests the hypothesis that DNA is an important target for Ang II-induced ROS leading to senescence via telomere-dependent and independent pathways. Reactive Oxygen Species 83-86 angiotensinogen Homo sapiens 68-74 17991883-7 2008 Inhibition by an AT1 receptor antagonist (losartan metabolite: E3174) or catalase, confirmed that Ang II-induced DNA damage was AT1 receptor-mediated, via the induction of ROS. Reactive Oxygen Species 172-175 angiotensinogen Homo sapiens 98-104 17991883-11 2008 These data demonstrate that Ang II-induced ROS-mediated DNA damage results in accelerated biological aging of hVSMCs via 2 mechanisms: (1) Acute SIPS, which is telomere independent, and (2) accelerated replicative senescence which is associated with accelerated telomere attrition. Reactive Oxygen Species 43-46 angiotensinogen Homo sapiens 28-34 18222975-6 2008 Our results showed that both ROS formation and hypertrophic responses induced by Ang II in cardiomyocytes were partially blocked by propofol. Reactive Oxygen Species 29-32 angiotensinogen Homo sapiens 81-87 18222975-8 2008 In addition, propofol also markedly attenuated Ang II-stimulated nuclear factor-kappaB (NF-kappaB) activation via a decrease in ROS production. Reactive Oxygen Species 128-131 angiotensinogen Homo sapiens 47-53 18287880-7 2008 During angiotensin II (AngII) activation, nox2 or p47 mRNA silencing decreased ROS production, while nox1 inhibition had no effect. Reactive Oxygen Species 79-82 angiotensinogen Homo sapiens 23-28 17482564-7 2007 These data suggest that activated intrarenal reactive oxygen species-angiotensinogen axis plays some roles in development of IgAN at the early stage and will provide supportive foundation of effectiveness of the renin-angiotensin system blockade in IgAN. Reactive Oxygen Species 45-68 angiotensinogen Homo sapiens 69-84 18197784-6 2008 Finally, we review the direct and indirect involvement of ROS and NOX in (tumor) angiogenesis through the regulation of different biologic systems such as vascular endothelial growth factor, angiotensin II, hypoxia-inducible factor, AP1, and inflammation. Reactive Oxygen Species 58-61 angiotensinogen Homo sapiens 191-205 17698051-0 2007 Role of mitochondria in angiotensin II-induced reactive oxygen species and mitogen-activated protein kinase activation. Reactive Oxygen Species 47-70 angiotensinogen Homo sapiens 24-38 17698051-1 2007 Peptide hormone Angiotensin II (Ang II) activates NAD(P)H oxidase, via AT1 receptors leading to increased generation of reactive oxygen species (ROS), such as the superoxide anion (O(2)(-)). Reactive Oxygen Species 120-143 angiotensinogen Homo sapiens 16-30 17698051-1 2007 Peptide hormone Angiotensin II (Ang II) activates NAD(P)H oxidase, via AT1 receptors leading to increased generation of reactive oxygen species (ROS), such as the superoxide anion (O(2)(-)). Reactive Oxygen Species 120-143 angiotensinogen Homo sapiens 32-38 17698051-1 2007 Peptide hormone Angiotensin II (Ang II) activates NAD(P)H oxidase, via AT1 receptors leading to increased generation of reactive oxygen species (ROS), such as the superoxide anion (O(2)(-)). Reactive Oxygen Species 145-148 angiotensinogen Homo sapiens 16-30 17698051-1 2007 Peptide hormone Angiotensin II (Ang II) activates NAD(P)H oxidase, via AT1 receptors leading to increased generation of reactive oxygen species (ROS), such as the superoxide anion (O(2)(-)). Reactive Oxygen Species 145-148 angiotensinogen Homo sapiens 32-38 17698051-4 2007 Accumulating evidence reveals that membrane-bound NAD(P)H oxidase is the main source responsible for Ang II-induced ROS generation. Reactive Oxygen Species 116-119 angiotensinogen Homo sapiens 101-107 17698051-5 2007 However, recent novel findings suggest that Ang II stimulation induces opening of mitochondrial K(ATP) channels, depolarizes mitochondrial potential (DeltaPsi(M)), and further amplifies ROS generation from mitochondria, resulting in redox-sensitive activation of MAPK. Reactive Oxygen Species 186-189 angiotensinogen Homo sapiens 44-50 17698051-6 2007 In this review, we discuss the possible mechanisms of Ang II-induced cardiac pharmacological preconditioning (PC), and focus on the role of mitochondrial K(ATP) channels, mitochondrial ROS production, and MAPK activation in response to Ang II stimulation. Reactive Oxygen Species 185-188 angiotensinogen Homo sapiens 54-60 17665974-5 2007 Thus, inhibition of the renal renin-angiotensin II-aldosterone system with angiotensin-converting enzyme inhibitor, angiotensin II type 1 receptor blocker or selective aldosterone inhibitor indirectly suppresses NADPH oxidase reducing renal ROS, proteinuria and glomerulosclerosis. Reactive Oxygen Species 241-244 angiotensinogen Homo sapiens 36-50 17665974-5 2007 Thus, inhibition of the renal renin-angiotensin II-aldosterone system with angiotensin-converting enzyme inhibitor, angiotensin II type 1 receptor blocker or selective aldosterone inhibitor indirectly suppresses NADPH oxidase reducing renal ROS, proteinuria and glomerulosclerosis. Reactive Oxygen Species 241-244 angiotensinogen Homo sapiens 116-130 17653214-3 2007 High glucose upregulates transforming growth factor-beta1 (TGF-beta1) and angiotensin II (Ang II) in renal cells and high glucose, TGF-beta1, and Ang II all generate and signal through ROS. Reactive Oxygen Species 185-188 angiotensinogen Homo sapiens 74-88 17653214-3 2007 High glucose upregulates transforming growth factor-beta1 (TGF-beta1) and angiotensin II (Ang II) in renal cells and high glucose, TGF-beta1, and Ang II all generate and signal through ROS. Reactive Oxygen Species 185-188 angiotensinogen Homo sapiens 90-96 17653214-3 2007 High glucose upregulates transforming growth factor-beta1 (TGF-beta1) and angiotensin II (Ang II) in renal cells and high glucose, TGF-beta1, and Ang II all generate and signal through ROS. Reactive Oxygen Species 185-188 angiotensinogen Homo sapiens 146-152 17631057-1 2007 Angiotensin II (Ang II), a potent vasoconstrictor, has been implicated in vascular inflammation through induction of reactive oxygen species (ROS) and pro-inflammatory genes. Reactive Oxygen Species 117-140 angiotensinogen Homo sapiens 0-22 17631057-1 2007 Angiotensin II (Ang II), a potent vasoconstrictor, has been implicated in vascular inflammation through induction of reactive oxygen species (ROS) and pro-inflammatory genes. Reactive Oxygen Species 142-145 angiotensinogen Homo sapiens 0-22 17556883-2 2007 Angiotensin II is a potent activator of NAD(P)H oxidase in the cardiovascular system, and augments production of reactive oxygen species. Reactive Oxygen Species 113-136 angiotensinogen Homo sapiens 0-14 17556883-3 2007 Numerous signaling pathways in response to angiotensin II are mediated by reactive oxygen species and oxidative stress is deeply associated with the progression of cardiovascular disease. Reactive Oxygen Species 74-97 angiotensinogen Homo sapiens 43-57 17556883-5 2007 RECENT FINDINGS: Recent studies have demonstrated novel molecular mechanisms of reactive oxygen species generation by angiotensin II and signaling pathways including cell proliferation, hypertrophy and apoptosis. Reactive Oxygen Species 80-103 angiotensinogen Homo sapiens 118-132 17586614-4 2007 Activation of the renin-angiotensin-aldosterone system and subsequent elevations in angiotensin II and aldosterone, as seen in cardiometabolic syndrome, contribute to altered insulin/IGF-1 signaling pathways and reactive oxygen species formation to induce endothelial dysfunction and cardiovascular disease. Reactive Oxygen Species 212-235 angiotensinogen Homo sapiens 84-98 17687073-0 2007 Angiotensin II-induced reactive oxygen species and the kidney. Reactive Oxygen Species 23-46 angiotensinogen Homo sapiens 0-14 17687073-2 2007 Accumulating evidence suggests that AngII stimulates intracellular formation of reactive oxygen species (ROS) such as the superoxide anion and hydrogen peroxide. Reactive Oxygen Species 80-103 angiotensinogen Homo sapiens 36-41 17687073-2 2007 Accumulating evidence suggests that AngII stimulates intracellular formation of reactive oxygen species (ROS) such as the superoxide anion and hydrogen peroxide. Reactive Oxygen Species 105-108 angiotensinogen Homo sapiens 36-41 17687073-3 2007 AngII activates several subunits of the membrane-bound multicomponent NAD(P)H oxidase and also increases ROS formation in the mitochondria. Reactive Oxygen Species 105-108 angiotensinogen Homo sapiens 0-5 17687073-8 2007 For example, AngII-mediated expression of p27(Kip1), a cell-cycle regulatory protein, and induction of tubular hypertrophy depend on the generation of ROS. Reactive Oxygen Species 151-154 angiotensinogen Homo sapiens 13-18 17556883-6 2007 In spite of these findings that strongly suggest the benefits of angiotensin II inhibition for cardiovascular disease, the clinical effects of angiotensin II-induced reactive oxygen species on the cardiovascular system are still controversial. Reactive Oxygen Species 166-189 angiotensinogen Homo sapiens 143-157 17556883-7 2007 SUMMARY: We focus on the effects of angiotensin II-induced oxidative stress on cardiovascular function and remodeling after discussing the source of reactive oxygen species and novel signaling pathways in response to reactive oxygen species. Reactive Oxygen Species 149-172 angiotensinogen Homo sapiens 36-50 17556883-7 2007 SUMMARY: We focus on the effects of angiotensin II-induced oxidative stress on cardiovascular function and remodeling after discussing the source of reactive oxygen species and novel signaling pathways in response to reactive oxygen species. Reactive Oxygen Species 217-240 angiotensinogen Homo sapiens 36-50 17709902-6 2007 Using the oxidation-sensitive dye dihydroethidium, we found that Klotho inhibited angiotensin II-induced reactive oxygen species production in HUVEC. Reactive Oxygen Species 105-128 angiotensinogen Homo sapiens 82-96 17303087-7 2007 Tanshinone IIA attenuated TNF-alpha, angiotensin II, H(2)O(2)-mediated reactive oxygen species (ROS) production. Reactive Oxygen Species 71-94 angiotensinogen Homo sapiens 37-51 17303087-7 2007 Tanshinone IIA attenuated TNF-alpha, angiotensin II, H(2)O(2)-mediated reactive oxygen species (ROS) production. Reactive Oxygen Species 96-99 angiotensinogen Homo sapiens 37-51 17143071-3 2007 Further, the angiotensin II-nitric oxide interaction can be modulated by reactive oxygen species. Reactive Oxygen Species 73-96 angiotensinogen Homo sapiens 13-27 17143071-4 2007 This review focuses on the angiotensin II-nitric oxide interaction and their modulation by reactive oxygen species in the control of renal blood flow. Reactive Oxygen Species 91-114 angiotensinogen Homo sapiens 27-41 17143071-7 2007 Angiotensin II-nitric oxide interactions are modulated by reactive oxygen species, as shown by angiotensin II type 1-mediated activation of superoxide and depression of antioxidant enzymes leading to reduced nitric oxide concentration - mechanisms that may be also important in angiotensin II-dependent hypertension. Reactive Oxygen Species 58-81 angiotensinogen Homo sapiens 0-14 17143071-7 2007 Angiotensin II-nitric oxide interactions are modulated by reactive oxygen species, as shown by angiotensin II type 1-mediated activation of superoxide and depression of antioxidant enzymes leading to reduced nitric oxide concentration - mechanisms that may be also important in angiotensin II-dependent hypertension. Reactive Oxygen Species 58-81 angiotensinogen Homo sapiens 95-109 17143071-7 2007 Angiotensin II-nitric oxide interactions are modulated by reactive oxygen species, as shown by angiotensin II type 1-mediated activation of superoxide and depression of antioxidant enzymes leading to reduced nitric oxide concentration - mechanisms that may be also important in angiotensin II-dependent hypertension. Reactive Oxygen Species 58-81 angiotensinogen Homo sapiens 278-292 17143071-9 2007 The interaction via angiotensin II type 1 is modulated by reactive oxygen species. Reactive Oxygen Species 58-81 angiotensinogen Homo sapiens 20-34 16860001-10 2006 CONDENSED ABSTRACT: Increased formation of reactive oxygen species, due to angiotensin II, contributes to vascular dysfunction. Reactive Oxygen Species 43-66 angiotensinogen Homo sapiens 75-89 17096009-2 2007 Acting via the type 1 receptor, Ang II initiates an inflammatory cascade of reduced nicotinamide-adenine dinucleotide phosphate oxidase, reactive oxygen species (ROS) and nuclear factor-kappaB, which mediates transcription and gene expression and increases adhesion molecules and chemokines. Reactive Oxygen Species 137-160 angiotensinogen Homo sapiens 32-38 17096009-2 2007 Acting via the type 1 receptor, Ang II initiates an inflammatory cascade of reduced nicotinamide-adenine dinucleotide phosphate oxidase, reactive oxygen species (ROS) and nuclear factor-kappaB, which mediates transcription and gene expression and increases adhesion molecules and chemokines. Reactive Oxygen Species 162-165 angiotensinogen Homo sapiens 32-38 17096009-6 2007 Ang II receptor blockers suppress mediators of inflammation, including ROS and C-reactive protein, and they increase expression of inhibitory kappaB (an inhibitor of nuclear factor-kappaB). Reactive Oxygen Species 71-74 angiotensinogen Homo sapiens 0-6 17824812-4 2007 Angiotensin II is a potent activator of NAD(P)H oxidase contributing to the production of reactive oxygen species. Reactive Oxygen Species 90-113 angiotensinogen Homo sapiens 0-14 17569300-5 2007 During normal pregnancy, AT1 receptors are found as monomers and are inactivated by reactive oxygen species (ROS) leading to lower Ang II sensitivity. Reactive Oxygen Species 84-107 angiotensinogen Homo sapiens 131-137 17569300-5 2007 During normal pregnancy, AT1 receptors are found as monomers and are inactivated by reactive oxygen species (ROS) leading to lower Ang II sensitivity. Reactive Oxygen Species 109-112 angiotensinogen Homo sapiens 131-137 18287671-4 2007 This association is mediated at least partially through interaction of angiotensin II (Ang II) with its receptor angiotensin receptor 1 (AT1R) in cardiovascular tissue, and subsequent activation of the nicotinamide adenine dinucleotide phosphate (NADPH) enzymatic complex, which finally leads to increased ROS production. Reactive Oxygen Species 306-309 angiotensinogen Homo sapiens 71-85 18287671-4 2007 This association is mediated at least partially through interaction of angiotensin II (Ang II) with its receptor angiotensin receptor 1 (AT1R) in cardiovascular tissue, and subsequent activation of the nicotinamide adenine dinucleotide phosphate (NADPH) enzymatic complex, which finally leads to increased ROS production. Reactive Oxygen Species 306-309 angiotensinogen Homo sapiens 87-93 16685192-4 2006 Reactive oxygen species and a network of signaling pathways mediate angiotensin II and cellular mechanisms that promote remodeling and inflammation. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 68-82 16915013-7 2006 The potential contribution of reactive oxygen species to the prohypertensive and proatherosclerotic effects of RAS is supported by evidence that nicotinamide adenine dinucleotide phosphate, reduced form oxidase is specifically stimulated by angiotensin II, an activity not shared by epinephrine. Reactive Oxygen Species 30-53 angiotensinogen Homo sapiens 241-255 16765337-4 2006 Ang II mediates many of its pleiotropic vascular effects through NAD(P)H oxidase-derived reactive oxygen species (ROS). Reactive Oxygen Species 89-112 angiotensinogen Homo sapiens 0-6 16765337-4 2006 Ang II mediates many of its pleiotropic vascular effects through NAD(P)H oxidase-derived reactive oxygen species (ROS). Reactive Oxygen Species 114-117 angiotensinogen Homo sapiens 0-6 16982630-2 2006 There is also evidence that angiotensin II (Ang II)-induced generation of ROS contributes to the development of insulin resistance in skeletal muscle, although the precise mechanisms remain unknown. Reactive Oxygen Species 74-77 angiotensinogen Homo sapiens 28-42 16982630-2 2006 There is also evidence that angiotensin II (Ang II)-induced generation of ROS contributes to the development of insulin resistance in skeletal muscle, although the precise mechanisms remain unknown. Reactive Oxygen Species 74-77 angiotensinogen Homo sapiens 44-50 16982630-3 2006 In the present study, we found that Ang II markedly enhanced NADPH oxidase activity and consequent ROS generation in L6 myotubes. Reactive Oxygen Species 99-102 angiotensinogen Homo sapiens 36-42 16982630-8 2006 These results suggest a pivotal role for NADPH oxidase activation and ROS generation in Ang II-induced inhibition of insulin signaling in skeletal muscle cells. Reactive Oxygen Species 70-73 angiotensinogen Homo sapiens 88-94 16879778-3 2006 Angiotensin II-induced generation of reactive oxygen species plays a key role in the pathophysiology of endothelial dysfunction by reducing NO bioavailability. Reactive Oxygen Species 37-60 angiotensinogen Homo sapiens 0-14 16750184-1 2006 OBJECTIVE: Angiotensin II stimulation increases the formation of reactive oxygen species (ROS), the phosphorylation of p38 mitogen-activated protein kinase (MAPK), and the expression of transforming growth factor beta (TGFbeta) in adult cardiomyocytes. Reactive Oxygen Species 65-88 angiotensinogen Homo sapiens 11-25 16750184-1 2006 OBJECTIVE: Angiotensin II stimulation increases the formation of reactive oxygen species (ROS), the phosphorylation of p38 mitogen-activated protein kinase (MAPK), and the expression of transforming growth factor beta (TGFbeta) in adult cardiomyocytes. Reactive Oxygen Species 90-93 angiotensinogen Homo sapiens 11-25 16750184-2 2006 The aim of this study was to determine the involvement of PI 3-kinase and to specify the participation of different isoforms in the angiotensin II-induced formation of ROS in comparison to the hypertrophic pathway triggered by alpha-adrenoceptor stimulation. Reactive Oxygen Species 168-171 angiotensinogen Homo sapiens 132-146 16750184-10 2006 CONCLUSION: Thus, our study identifies an involvement of PI 3-kinase in the angiotensin II-induced formation of ROS and provides a biochemical basis for ligand-specific responses for angiotensin II and alpha-adrenoceptor stimulation as relates to hypertrophy. Reactive Oxygen Species 112-115 angiotensinogen Homo sapiens 76-90 16910759-9 2006 Furthermore, NADPH-oxidase-derived ROS partly contribute to flow-dependent dilatation and may offset angiotensin II-induced constriction of cerebral arteries, consistent with the hypothesis that NADPH-oxidase-derived ROS may play a physiologic role in the control of cerebrovascular tone. Reactive Oxygen Species 35-38 angiotensinogen Homo sapiens 101-115 16910759-9 2006 Furthermore, NADPH-oxidase-derived ROS partly contribute to flow-dependent dilatation and may offset angiotensin II-induced constriction of cerebral arteries, consistent with the hypothesis that NADPH-oxidase-derived ROS may play a physiologic role in the control of cerebrovascular tone. Reactive Oxygen Species 217-220 angiotensinogen Homo sapiens 101-115 16505203-7 2006 The production of ROS increased in response to Ang II treatment (DeltaROS respect to control: 68+/-15 fluorescence units; P<0.05). Reactive Oxygen Species 18-21 angiotensinogen Homo sapiens 47-53 16768130-2 2006 Activation of AT1 receptors by angiotensin II initiates a complex signaling cascade via in part reactive oxygen species produced by the enzyme NADPH oxidase in blood vessels and induces vasoconstriction, vascular proliferation, and inflammation leading to cerebrovascular insufficiency. Reactive Oxygen Species 96-119 angiotensinogen Homo sapiens 31-45 16948472-7 2006 Furthermore, PEDF blocked the Ang II-induced reactive oxygen species (ROS) generation and NADPH oxidase activity in MOLT-3 T cells. Reactive Oxygen Species 45-68 angiotensinogen Homo sapiens 30-36 16948472-7 2006 Furthermore, PEDF blocked the Ang II-induced reactive oxygen species (ROS) generation and NADPH oxidase activity in MOLT-3 T cells. Reactive Oxygen Species 70-73 angiotensinogen Homo sapiens 30-36 16948472-8 2006 These results demonstrate that PEDF inhibits the Ang II-induced T cell proliferation by blocking autocrine production of IL-2 via suppression of NADPH oxidase-mediated ROS generation. Reactive Oxygen Species 168-171 angiotensinogen Homo sapiens 49-55 16724941-4 2006 The ROS production induced by AngII activates downstream ROS-sensitive kinases that are critical in mediating cardiovascular remodeling. Reactive Oxygen Species 4-7 angiotensinogen Homo sapiens 30-35 16724941-5 2006 Recent advances in gene transfer/knockout techniques have lead to numerous in vitro and in vivo studies that identify the potential components and mechanisms of ROS signal transduction by AngII which promote cardiovascular remodeling. Reactive Oxygen Species 161-164 angiotensinogen Homo sapiens 188-193 16724941-6 2006 In this review, we will focus our discussion on the signal transduction research elucidating ROS production and function induced by AngII using currently available molecular biotechnologies. Reactive Oxygen Species 93-96 angiotensinogen Homo sapiens 132-137 16249273-0 2006 Angiotensin II stimulation of VEGF mRNA translation requires production of reactive oxygen species. Reactive Oxygen Species 75-98 angiotensinogen Homo sapiens 0-14 16724941-0 2006 Current understanding of the mechanism and role of ROS in angiotensin II signal transduction. Reactive Oxygen Species 51-54 angiotensinogen Homo sapiens 58-72 16724941-3 2006 Angiotensin II (AngII), a potent cardiovascular pathogen, stimulates ROS production through vascular NADPH oxidases. Reactive Oxygen Species 69-72 angiotensinogen Homo sapiens 0-14 16724941-3 2006 Angiotensin II (AngII), a potent cardiovascular pathogen, stimulates ROS production through vascular NADPH oxidases. Reactive Oxygen Species 69-72 angiotensinogen Homo sapiens 16-21 16505203-8 2006 The Ang II-induced PIE and ROS production were blocked by the Ang II type 1 receptor blocker losartan, the nonselective ET-1 receptor blocker TAK044, the selective ETA receptor blocker BQ-123, or the ROS scavenger N-(2-mercapto-propionyl)glycine. Reactive Oxygen Species 27-30 angiotensinogen Homo sapiens 4-10 16505203-8 2006 The Ang II-induced PIE and ROS production were blocked by the Ang II type 1 receptor blocker losartan, the nonselective ET-1 receptor blocker TAK044, the selective ETA receptor blocker BQ-123, or the ROS scavenger N-(2-mercapto-propionyl)glycine. Reactive Oxygen Species 27-30 angiotensinogen Homo sapiens 62-68 16505203-8 2006 The Ang II-induced PIE and ROS production were blocked by the Ang II type 1 receptor blocker losartan, the nonselective ET-1 receptor blocker TAK044, the selective ETA receptor blocker BQ-123, or the ROS scavenger N-(2-mercapto-propionyl)glycine. Reactive Oxygen Species 200-203 angiotensinogen Homo sapiens 4-10 16505203-12 2006 We conclude that the PIE after exposure to 1 nmol/L Ang II is due to endogenous ET-1 acting through the ETA receptor and triggering ROS production, Na+/H+ exchanger stimulation, and Na+/Ca2+ exchanger reverse mode activation. Reactive Oxygen Species 132-135 angiotensinogen Homo sapiens 52-58 16481883-5 2006 Among the intracellular signals involved in angiotensin II-induced inflammation, the production of reactive oxygen species and the activation of nuclear factor-kappaB are the best known. Reactive Oxygen Species 99-122 angiotensinogen Homo sapiens 44-58 16778463-7 2006 Though reactive oxygen species in a small amount are produced constantly, the decreased metabolic turnover of homocysteine, poor performance of antioxidants or high level of angiotensin II alters the balance between production of free radicals and their neutralization. Reactive Oxygen Species 7-30 angiotensinogen Homo sapiens 174-188 16472178-4 2006 In VSMCs, AngII also induces the generation of intracellular reactive oxygen species (ROS), which play critical roles in activation and modulation of above signal transduction. Reactive Oxygen Species 61-84 angiotensinogen Homo sapiens 10-15 16472178-4 2006 In VSMCs, AngII also induces the generation of intracellular reactive oxygen species (ROS), which play critical roles in activation and modulation of above signal transduction. Reactive Oxygen Species 86-89 angiotensinogen Homo sapiens 10-15 16472178-8 2006 In this review, we focus on the recent findings that suggest the existence of novel signaling mechanisms whereby AngII mediates processes, such as activation of receptor or non-receptor tyrosine kinases and ROS, as well as cross-talk between insulin and NO signal transduction in VSMCs and ECs. Reactive Oxygen Species 207-210 angiotensinogen Homo sapiens 113-118 16601568-2 2006 RESULTS: AT1-receptor activation by angiotensin II is not only involved in the regulation of blood pressure, water and sodium homeostasis, and control of other neurohumoral systems, but also leads to excessive production of reactive oxygen species and to hypertrophy, proliferation, migration, and apoptosis of vascular cells. Reactive Oxygen Species 224-247 angiotensinogen Homo sapiens 36-50 16340217-6 2006 Urocortin (10(-8) M) potently suppressed the generation of angiotensin II-induced reactive oxygen species (ROS) in HUVECs. Reactive Oxygen Species 82-105 angiotensinogen Homo sapiens 59-73 16340217-6 2006 Urocortin (10(-8) M) potently suppressed the generation of angiotensin II-induced reactive oxygen species (ROS) in HUVECs. Reactive Oxygen Species 107-110 angiotensinogen Homo sapiens 59-73 16224073-0 2005 The regulation of sympathetic nerve activity by angiotensin II involves reactive oxygen species and MAPK. Reactive Oxygen Species 72-95 angiotensinogen Homo sapiens 48-62 16243586-2 2005 Recent reports have suggested that in addition to the classical pathways involved in transducing responses to receptor activation, formation of reactive oxygen species by angiotensin II may also be involved. Reactive Oxygen Species 144-167 angiotensinogen Homo sapiens 171-185 16172434-2 2005 An increasing number of studies have demonstrated that reactive oxygen species are involved in many of the vascular responses to angiotensin II. Reactive Oxygen Species 55-78 angiotensinogen Homo sapiens 129-143 16174288-5 2005 PKC, TGF-beta1, Ang II, and AGE also induce cellular ROS and signal through ROS leading to enhanced ECM synthesis. Reactive Oxygen Species 53-56 angiotensinogen Homo sapiens 16-22 16174288-5 2005 PKC, TGF-beta1, Ang II, and AGE also induce cellular ROS and signal through ROS leading to enhanced ECM synthesis. Reactive Oxygen Species 76-79 angiotensinogen Homo sapiens 16-22 16115036-0 2005 Reactive oxygen species as mediators of calcium signaling by angiotensin II: implications in vascular physiology and pathophysiology. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 61-75 16115037-3 2005 Angiotensin II (AngII), a potent cardiovascular pathogen, stimulates ROS production through the G protein-coupled AngII type 1 receptor expressed in its target organs, such as vascular tissues, heart, and kidney. Reactive Oxygen Species 69-72 angiotensinogen Homo sapiens 0-14 16115037-3 2005 Angiotensin II (AngII), a potent cardiovascular pathogen, stimulates ROS production through the G protein-coupled AngII type 1 receptor expressed in its target organs, such as vascular tissues, heart, and kidney. Reactive Oxygen Species 69-72 angiotensinogen Homo sapiens 16-21 16115037-3 2005 Angiotensin II (AngII), a potent cardiovascular pathogen, stimulates ROS production through the G protein-coupled AngII type 1 receptor expressed in its target organs, such as vascular tissues, heart, and kidney. Reactive Oxygen Species 69-72 angiotensinogen Homo sapiens 114-119 16115037-4 2005 Recent accumulating evidence indicates that through ROS production, AngII activates downstream ROS-sensitive kinases that are critical in mediating cardiovascular remodeling. Reactive Oxygen Species 52-55 angiotensinogen Homo sapiens 68-73 16115037-4 2005 Recent accumulating evidence indicates that through ROS production, AngII activates downstream ROS-sensitive kinases that are critical in mediating cardiovascular remodeling. Reactive Oxygen Species 95-98 angiotensinogen Homo sapiens 68-73 15859946-8 2005 As compared with the normal condition, stimulation of PCs with angiotensin II or high glucose induced: (i) an increase in ROS production and NAD(P)H oxidase activity, and (ii) an up-regulation of p22(phox) mRNA and protein expression. Reactive Oxygen Species 122-125 angiotensinogen Homo sapiens 63-77 15976327-4 2005 METHODS AND RESULTS: Knockdown of Cav1 protein by small interfering RNA (siRNA) inhibits Ang II-stimulated Rac1 activation and membrane translocation, H2O2 production, ROS-dependent epidermal growth factor receptor (EGF-R) transactivation, and subsequent phosphorylation of Akt without affecting ROS-independent extracellular signal-regulated kinase 1/2 phosphorylation. Reactive Oxygen Species 296-299 angiotensinogen Homo sapiens 89-95 15976327-10 2005 CONCLUSIONS: Cav1 plays an essential role in AT1R targeting into Cav1-enriched lipid rafts and Rac1 activation, which are required for proper organization of ROS-dependent Ang II signaling linked to VSMC hypertrophy. Reactive Oxygen Species 158-161 angiotensinogen Homo sapiens 172-178 16341292-1 2005 It is now well established that the activation of the renin-angiotensin system (RAS) is involved in the onset and progression of cardiovascular and renal diseases, and that its main effector, angiotensin II (Ang II) has major pro-inflammatory activity that induces the expression of cytokines, chemokines, adhesion molecules, growth factors and reactive oxygen species. Reactive Oxygen Species 345-368 angiotensinogen Homo sapiens 192-206 16341292-1 2005 It is now well established that the activation of the renin-angiotensin system (RAS) is involved in the onset and progression of cardiovascular and renal diseases, and that its main effector, angiotensin II (Ang II) has major pro-inflammatory activity that induces the expression of cytokines, chemokines, adhesion molecules, growth factors and reactive oxygen species. Reactive Oxygen Species 345-368 angiotensinogen Homo sapiens 208-214 15944212-6 2005 The generation of reactive oxygen species (ROS) in endothelial cells stimulated with Ang-II was inhibited significantly by the three alkaloids tested. Reactive Oxygen Species 18-41 angiotensinogen Homo sapiens 85-91 16116043-5 2005 In the current studies, we tested the hypothesis that the effects of Ang II on central SNS are mediated by reactive oxygen species. Reactive Oxygen Species 107-130 angiotensinogen Homo sapiens 69-75 15944212-6 2005 The generation of reactive oxygen species (ROS) in endothelial cells stimulated with Ang-II was inhibited significantly by the three alkaloids tested. Reactive Oxygen Species 43-46 angiotensinogen Homo sapiens 85-91 29350806-6 2005 The generation of reactive oxygen species (ROS) in endothelial cells stimulated with Ang-II was inhibited significantly by the three alkaloids tested. Reactive Oxygen Species 18-41 angiotensinogen Homo sapiens 85-91 29350806-6 2005 The generation of reactive oxygen species (ROS) in endothelial cells stimulated with Ang-II was inhibited significantly by the three alkaloids tested. Reactive Oxygen Species 43-46 angiotensinogen Homo sapiens 85-91 16125525-5 2005 To sum it up, Flu administration had a beneficial effect on AII-triggered reactive oxygen species generation; it resulted in partial restoration of signaling processes and of membrane composition, but membrane fluidity remained unchanged. Reactive Oxygen Species 74-97 angiotensinogen Homo sapiens 60-63 15998260-4 2005 Recently, we reported that lysophosphatidylcholine, a major bioactive product of oxidized low-density lipoprotein, and angiotensin II, a vasoactive hormone and a potent inducer of reactive oxygen species (ROS), negatively regulate insulin signaling in vascular smooth muscle cells (VSMCs). Reactive Oxygen Species 180-203 angiotensinogen Homo sapiens 119-133 15802301-4 2005 Experimental data showed that green tea polyphenols could inhibit angiotensin II-induced reactive oxygen species production. Reactive Oxygen Species 89-112 angiotensinogen Homo sapiens 66-80 15944340-1 2005 Antioxidants seem to inhibit angiotensin II (Ang II) actions by consuming stimulated reactive oxygen species. Reactive Oxygen Species 85-108 angiotensinogen Homo sapiens 29-43 15944340-1 2005 Antioxidants seem to inhibit angiotensin II (Ang II) actions by consuming stimulated reactive oxygen species. Reactive Oxygen Species 85-108 angiotensinogen Homo sapiens 45-51 15998260-4 2005 Recently, we reported that lysophosphatidylcholine, a major bioactive product of oxidized low-density lipoprotein, and angiotensin II, a vasoactive hormone and a potent inducer of reactive oxygen species (ROS), negatively regulate insulin signaling in vascular smooth muscle cells (VSMCs). Reactive Oxygen Species 205-208 angiotensinogen Homo sapiens 119-133 16026320-3 2005 Evidence accumulated in the last decade strongly supports the notion that ROS are generated in the vasculature mainly by NAD(P)H oxidase in a mechanism that is angiotensin II-dependent. Reactive Oxygen Species 74-77 angiotensinogen Homo sapiens 160-174 16202699-4 2005 At some point, angiotensin II activates additional mechanisms responsible for sustained increased blood pressure including sodium retention, endothelial dysfunction, and vasoconstriction related to production of reactive oxygen species. Reactive Oxygen Species 212-235 angiotensinogen Homo sapiens 15-29 15917731-7 2005 Ang II, via the type 1 (AT1) receptors, enhances the production of reactive oxygen species (ROS) through stimulation of NAD(P)H oxidase in the vascular wall. Reactive Oxygen Species 67-90 angiotensinogen Homo sapiens 0-6 15802620-0 2005 Mechanisms of reactive oxygen species-dependent downregulation of insulin receptor substrate-1 by angiotensin II. Reactive Oxygen Species 14-37 angiotensinogen Homo sapiens 98-112 15802620-10 2005 CONCLUSIONS: Thus, angiotensin II decreases IRS-1 protein levels in VSMCs via Src, PDK1, and reactive oxygen species-mediated phosphorylation of IRS-1 on Ser307 and subsequent proteasome-dependent degradation. Reactive Oxygen Species 93-116 angiotensinogen Homo sapiens 19-33 16037256-3 2005 As presented here, the stimulation of cultured monocytes by phorbol-12-myristate-13-acetate (TPA), an activator of protein kinase C that can mimic the effects of high glucose, angiotensin II, and other physiological stimuli, leads to cellular ROS generation and concomitant formation of intracellular CML. Reactive Oxygen Species 243-246 angiotensinogen Homo sapiens 176-190 15917731-7 2005 Ang II, via the type 1 (AT1) receptors, enhances the production of reactive oxygen species (ROS) through stimulation of NAD(P)H oxidase in the vascular wall. Reactive Oxygen Species 92-95 angiotensinogen Homo sapiens 0-6 15890031-3 2005 The discovery of reactive oxygen species production by angiotensin II in vascular smooth muscle cells via the activation of NAD(P)H oxidase promoted studies of redox control of growth factor signaling. Reactive Oxygen Species 17-40 angiotensinogen Homo sapiens 55-69 15965074-4 2005 Treatment of mesangial cells with Ang II (100 nM) increased production of reactive oxygen species (ROS). Reactive Oxygen Species 74-97 angiotensinogen Homo sapiens 34-40 15965074-4 2005 Treatment of mesangial cells with Ang II (100 nM) increased production of reactive oxygen species (ROS). Reactive Oxygen Species 99-102 angiotensinogen Homo sapiens 34-40 15965074-7 2005 Because increased ROS generation by Ang II may activate the PI-3K-PKB/Akt signaling pathway, these results suggest that Ang II may stimulate a ROS-dependent activation of the PI-3K-PKB/Akt pathway, which leads to HIF-1alpha accumulation. Reactive Oxygen Species 18-21 angiotensinogen Homo sapiens 36-42 15965074-7 2005 Because increased ROS generation by Ang II may activate the PI-3K-PKB/Akt signaling pathway, these results suggest that Ang II may stimulate a ROS-dependent activation of the PI-3K-PKB/Akt pathway, which leads to HIF-1alpha accumulation. Reactive Oxygen Species 18-21 angiotensinogen Homo sapiens 120-126 15965074-7 2005 Because increased ROS generation by Ang II may activate the PI-3K-PKB/Akt signaling pathway, these results suggest that Ang II may stimulate a ROS-dependent activation of the PI-3K-PKB/Akt pathway, which leads to HIF-1alpha accumulation. Reactive Oxygen Species 143-146 angiotensinogen Homo sapiens 36-42 15965074-7 2005 Because increased ROS generation by Ang II may activate the PI-3K-PKB/Akt signaling pathway, these results suggest that Ang II may stimulate a ROS-dependent activation of the PI-3K-PKB/Akt pathway, which leads to HIF-1alpha accumulation. Reactive Oxygen Species 143-146 angiotensinogen Homo sapiens 120-126 15820256-7 2005 This correlated with a decrease in TNF-alpha- or angiotensin-II-induced ROS production assayed by DCF fluorescence. Reactive Oxygen Species 72-75 angiotensinogen Homo sapiens 49-63 18220595-5 2005 Recent findings indicate that HG and Ang II activate intracellular processes, including the polyol pathway and the generation of reactive oxygen species. Reactive Oxygen Species 129-152 angiotensinogen Homo sapiens 37-43 15841036-4 2005 Apart from its potent vasoconstrictor actions, the renin-angiotensin system (RAS) that generates angiotensin II has several novel functions-stimulation and inhibition of cell proliferation; induction of apoptosis; generation of reactive oxygen species; regulation of hormone secretion; and proinflammatory and profibrogenic actions. Reactive Oxygen Species 228-251 angiotensinogen Homo sapiens 97-111 15746442-2 2005 However, the intracellular mechanism by which reactive oxygen species (ROS) signaling regulates neuronal Ang II actions remains to be elucidated. Reactive Oxygen Species 46-69 angiotensinogen Homo sapiens 105-111 15746442-2 2005 However, the intracellular mechanism by which reactive oxygen species (ROS) signaling regulates neuronal Ang II actions remains to be elucidated. Reactive Oxygen Species 71-74 angiotensinogen Homo sapiens 105-111 15746442-3 2005 In the present study, we have used neuronal cells in primary cultures from the hypothalamus and brain stem areas to study the role of ROS on the cellular actions of Ang II. Reactive Oxygen Species 134-137 angiotensinogen Homo sapiens 165-171 15746442-7 2005 Extracellular application of the ROS scavenger, Tempol, attenuated the Ang II-induced increase in neuronal firing rate by 70%. Reactive Oxygen Species 33-36 angiotensinogen Homo sapiens 71-77 15746442-11 2005 These observations demonstrate, for the first time, that Ang II regulates neuronal activity via a series of events that includes ROS generation and inhibition of I(Kv). Reactive Oxygen Species 129-132 angiotensinogen Homo sapiens 57-63 15638745-8 2005 Secondly, the mechanisms for the beneficial effects of angiotensin II receptor blockers studied in model systems and in humans, including possible involvement in the formation of reactive oxygen species by mononuclear cells, are presented. Reactive Oxygen Species 179-202 angiotensinogen Homo sapiens 55-69 15670768-2 2005 Since reactive oxygen species (ROS) induce MMP-2 and angiotensin II (ANG II) enhances NADPH-oxidase-dependent ROS formation, we assessed whether ANG II induces MMP-2 in a NADPH-oxidase-dependent manner. Reactive Oxygen Species 110-113 angiotensinogen Homo sapiens 69-75 15618548-7 2005 Intracellular ROS generation in response to LY83583 (O2 generator) or exogenous H2O2 and Ang II-induced ERK1/2 activation were unaltered by cytochalasin. Reactive Oxygen Species 14-17 angiotensinogen Homo sapiens 89-95 15618548-8 2005 CONCLUSIONS: The p47phox:actin interaction, through cortactin, plays an important role in Ang II-mediated site-directed assembly of functionally active NAD(P)H oxidase, ROS generation, and activation of redox-sensitive p38MAP kinase and Akt, but not ERK1/2. Reactive Oxygen Species 169-172 angiotensinogen Homo sapiens 90-96 16425978-4 2005 Azelnidipine, but not nitrendipine, the other popular DHFP completely inhibited the Ang II-induced ROS generation in ECs. Reactive Oxygen Species 99-102 angiotensinogen Homo sapiens 84-90 15273829-5 2004 Growing evidence indicates that Ang II induces its pleiotropic vascular effects through NADPH-driven generation of reactive oxygen species (ROS). Reactive Oxygen Species 115-138 angiotensinogen Homo sapiens 32-38 15780486-6 2005 Angiotensin II stimulates nicotinamide adenine dinucleotide phosphate/nicotinamide adenine dinucleotide oxidase in endothelium, smooth muscle cells, and the adventitia of blood vessel to generate reactive oxygen species, leading to endothelial dysfunction, growth, and inflammation, upregulation of endothelin-1, adhesion molecules, nuclear factor-kappa B, and other inflammatory mediators, as well as increased breakdown of nitric oxide and uncoupling of nitric oxide synthase, contribute to the progression of vascular disease and atherogenesis. Reactive Oxygen Species 196-219 angiotensinogen Homo sapiens 0-14 15770925-0 2005 Angiotensin II mediates high glucose-induced TGF-beta1 and fibronectin upregulation in HPMC through reactive oxygen species. Reactive Oxygen Species 100-123 angiotensinogen Homo sapiens 0-14 15606719-8 2004 In fact, it has been shown that angiotensin II is involved in almost every pathophysiological process implicated in the development of diabetic nephropathy (haemodynamic changes, hypertrophy, extracellular matrix accumulation, growth factor/cytokine induction, ROS formation, podocyte damage, proteinuria, interstitial inflammation). Reactive Oxygen Species 261-264 angiotensinogen Homo sapiens 32-46 15466667-8 2004 Ang II stimulated the intracellular generation of reactive oxygen species (ROS), and this effect was also attenuated by pioglitazone. Reactive Oxygen Species 50-73 angiotensinogen Homo sapiens 0-6 15466667-8 2004 Ang II stimulated the intracellular generation of reactive oxygen species (ROS), and this effect was also attenuated by pioglitazone. Reactive Oxygen Species 75-78 angiotensinogen Homo sapiens 0-6 15084475-6 2004 Angiotensin II-induced phosphorylation of MAPKAPK-2 is also attenuated by SB-203580, as well as by inhibitors of ROS. Reactive Oxygen Species 113-116 angiotensinogen Homo sapiens 0-14 16215641-1 2005 NAD(P)H oxidase is one of the most important sources of reactive oxygen species and has been demonstrated to be upregulated by angiotensin II in the kidney. Reactive Oxygen Species 56-79 angiotensinogen Homo sapiens 127-141 15763950-5 2004 Intracellular ROS, as generated by the angiotensin II (Ang II)-activated NADPH oxidase, did not increase the oxidation of H2-calcein but increased the oxidation of H2-DCF by approximately 50%. Reactive Oxygen Species 14-17 angiotensinogen Homo sapiens 39-53 15763950-5 2004 Intracellular ROS, as generated by the angiotensin II (Ang II)-activated NADPH oxidase, did not increase the oxidation of H2-calcein but increased the oxidation of H2-DCF by approximately 50%. Reactive Oxygen Species 14-17 angiotensinogen Homo sapiens 55-61 15273829-5 2004 Growing evidence indicates that Ang II induces its pleiotropic vascular effects through NADPH-driven generation of reactive oxygen species (ROS). Reactive Oxygen Species 140-143 angiotensinogen Homo sapiens 32-38 15273829-12 2004 The present review focuses on the biology of ROS in Ang II signaling in vascular cells and discusses how oxidative stress contributes to vascular damage in cardiovascular disease. Reactive Oxygen Species 45-48 angiotensinogen Homo sapiens 52-58 15203192-1 2004 Reactive oxygen species (ROS) have been shown to mediate the effects of several growth factors and vasoactive peptides, such as epidermal growth factor, platelet-derived growth factor, and angiotensin II (AII). Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 189-203 15203192-1 2004 Reactive oxygen species (ROS) have been shown to mediate the effects of several growth factors and vasoactive peptides, such as epidermal growth factor, platelet-derived growth factor, and angiotensin II (AII). Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 205-208 15203192-1 2004 Reactive oxygen species (ROS) have been shown to mediate the effects of several growth factors and vasoactive peptides, such as epidermal growth factor, platelet-derived growth factor, and angiotensin II (AII). Reactive Oxygen Species 25-28 angiotensinogen Homo sapiens 189-203 15203192-1 2004 Reactive oxygen species (ROS) have been shown to mediate the effects of several growth factors and vasoactive peptides, such as epidermal growth factor, platelet-derived growth factor, and angiotensin II (AII). Reactive Oxygen Species 25-28 angiotensinogen Homo sapiens 205-208 15201324-2 2004 In vascular cells, reactive oxygen species (ROS) generated by the enzyme NADPH oxidase play a major role in AngII signaling. Reactive Oxygen Species 19-42 angiotensinogen Homo sapiens 108-113 15142861-2 2004 Full expression of angiotensin II (Ang II) signaling in vascular smooth muscle cells (VSMCs) is dependent on the reactive oxygen species (ROS) derived from nicotinamide-adenine dinucleotide phosphate (NAD(P)H) oxidase and the dynamic association of the Ang II type 1 receptor (AT1R) with caveolae/lipid rafts. Reactive Oxygen Species 113-136 angiotensinogen Homo sapiens 19-33 15142861-2 2004 Full expression of angiotensin II (Ang II) signaling in vascular smooth muscle cells (VSMCs) is dependent on the reactive oxygen species (ROS) derived from nicotinamide-adenine dinucleotide phosphate (NAD(P)H) oxidase and the dynamic association of the Ang II type 1 receptor (AT1R) with caveolae/lipid rafts. Reactive Oxygen Species 113-136 angiotensinogen Homo sapiens 35-41 15142861-2 2004 Full expression of angiotensin II (Ang II) signaling in vascular smooth muscle cells (VSMCs) is dependent on the reactive oxygen species (ROS) derived from nicotinamide-adenine dinucleotide phosphate (NAD(P)H) oxidase and the dynamic association of the Ang II type 1 receptor (AT1R) with caveolae/lipid rafts. Reactive Oxygen Species 138-141 angiotensinogen Homo sapiens 19-33 15142861-2 2004 Full expression of angiotensin II (Ang II) signaling in vascular smooth muscle cells (VSMCs) is dependent on the reactive oxygen species (ROS) derived from nicotinamide-adenine dinucleotide phosphate (NAD(P)H) oxidase and the dynamic association of the Ang II type 1 receptor (AT1R) with caveolae/lipid rafts. Reactive Oxygen Species 138-141 angiotensinogen Homo sapiens 35-41 15123696-1 2004 Angiotensin II (AII) increases production of reactive oxygen species from NAD(P)H oxidase, a response that contributes to vascular hypertrophy. Reactive Oxygen Species 45-68 angiotensinogen Homo sapiens 0-14 15123696-1 2004 Angiotensin II (AII) increases production of reactive oxygen species from NAD(P)H oxidase, a response that contributes to vascular hypertrophy. Reactive Oxygen Species 45-68 angiotensinogen Homo sapiens 16-19 15027896-10 2004 These results demonstrate that Ang II stimulates ERK1/ERK2 by AA and Nox4-derived reactive oxygen species, suggesting that these molecules act as downstream signal transducers of Ang II in the signalling pathway linking the Ang II receptor AT1 to ERK1/ERK2 activation. Reactive Oxygen Species 82-105 angiotensinogen Homo sapiens 31-37 15027896-10 2004 These results demonstrate that Ang II stimulates ERK1/ERK2 by AA and Nox4-derived reactive oxygen species, suggesting that these molecules act as downstream signal transducers of Ang II in the signalling pathway linking the Ang II receptor AT1 to ERK1/ERK2 activation. Reactive Oxygen Species 82-105 angiotensinogen Homo sapiens 179-185 15027896-10 2004 These results demonstrate that Ang II stimulates ERK1/ERK2 by AA and Nox4-derived reactive oxygen species, suggesting that these molecules act as downstream signal transducers of Ang II in the signalling pathway linking the Ang II receptor AT1 to ERK1/ERK2 activation. Reactive Oxygen Species 82-105 angiotensinogen Homo sapiens 179-185 15027896-11 2004 This pathway involving AA, Rac1, Nox4, reactive oxygen species and ERK1/ERK2 may play an important role in Ang II-induced mesangial cell hypertrophy. Reactive Oxygen Species 39-62 angiotensinogen Homo sapiens 107-113 15201324-2 2004 In vascular cells, reactive oxygen species (ROS) generated by the enzyme NADPH oxidase play a major role in AngII signaling. Reactive Oxygen Species 44-47 angiotensinogen Homo sapiens 108-113 15201324-7 2004 In parallel experiments using patch clamp of dissociated NTS neurons anterogradely labeled via the vagus, we found that AngII potentiates the L-type Ca2+ currents, an effect mediated by AT1 receptors and abolished by the ROS scavenger Mn(III) tetrakis (4-benzoic acid) porphyrin chloride. Reactive Oxygen Species 221-224 angiotensinogen Homo sapiens 120-125 15201324-9 2004 The results provide evidence that NADPH oxidase-derived ROS are involved in the effects of AngII on Ca2+ influx in NTS neurons receiving vagal afferents and support the notion that ROS are important signaling molecules in central autonomic networks. Reactive Oxygen Species 56-59 angiotensinogen Homo sapiens 91-96 15201324-9 2004 The results provide evidence that NADPH oxidase-derived ROS are involved in the effects of AngII on Ca2+ influx in NTS neurons receiving vagal afferents and support the notion that ROS are important signaling molecules in central autonomic networks. Reactive Oxygen Species 181-184 angiotensinogen Homo sapiens 91-96 15159288-8 2004 Preincubating the cells with the MR blocker spironolactone (10(-6) mol/L) abolished Ang II-induced ROS generation, EGFR transactivation, and ERK1/2 phosphorylation. Reactive Oxygen Species 99-102 angiotensinogen Homo sapiens 84-90 15159288-10 2004 Oxygen radicals, the MR, and the EGFR play a role in early signaling induced by Ang II and Ald in VSMCs. Reactive Oxygen Species 0-15 angiotensinogen Homo sapiens 80-86 15167449-1 2004 OBJECTIVE: The role of reactive oxygen species (ROS) in mitogen-activated protein kinase (MAPK) signaling by angiotensin (Ang) II and endothelin-1 (ET-1) in human vascular smooth muscle cells (VSMC) was investigated. Reactive Oxygen Species 23-46 angiotensinogen Homo sapiens 109-129 15167449-1 2004 OBJECTIVE: The role of reactive oxygen species (ROS) in mitogen-activated protein kinase (MAPK) signaling by angiotensin (Ang) II and endothelin-1 (ET-1) in human vascular smooth muscle cells (VSMC) was investigated. Reactive Oxygen Species 48-51 angiotensinogen Homo sapiens 109-129 14730203-0 2004 Role of reactive oxygen species-sensitive extracellular signal-regulated kinase pathway in angiotensin II-induced endothelin-1 gene expression in vascular endothelial cells. Reactive Oxygen Species 8-31 angiotensinogen Homo sapiens 91-105 14652666-1 2004 Reactive oxygen species (ROS) are involved in the transcriptional response to angiotensin (ANG) II. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 78-98 14652666-1 2004 Reactive oxygen species (ROS) are involved in the transcriptional response to angiotensin (ANG) II. Reactive Oxygen Species 25-28 angiotensinogen Homo sapiens 78-98 14652666-4 2004 We investigated the role of ANG II and platelet-derived growth factor (PDGF) AA induced ROS generation derived from p22phox-containing NAD(P)H oxidase in the activation of activator protein (AP) 1 in human vascular smooth muscle cells (SMCs). Reactive Oxygen Species 88-91 angiotensinogen Homo sapiens 28-34 14652666-5 2004 Both ANG II and PDGF AA induced ROS generation in SMCs which was angiotensin type 1 receptor and PDGF alpha receptor dependent. Reactive Oxygen Species 32-35 angiotensinogen Homo sapiens 5-11 14652666-9 2004 These findings demonstrate that AP-1 activation in human SMCs in response to ANG II and PDGF AA is mediated via generation of p22phox-dependent ROS. Reactive Oxygen Species 144-147 angiotensinogen Homo sapiens 77-83 14730203-2 2004 Ang II also stimulates the generation of reactive oxygen species (ROS) within vascular endothelial cells. Reactive Oxygen Species 41-64 angiotensinogen Homo sapiens 0-6 14730203-2 2004 Ang II also stimulates the generation of reactive oxygen species (ROS) within vascular endothelial cells. Reactive Oxygen Species 66-69 angiotensinogen Homo sapiens 0-6 14730203-3 2004 However, whether ROS are involved in Ang II-induced ET-1 gene expression, and the related intracellular mechanisms occurring within vascular endothelial cells remain unclear. Reactive Oxygen Species 17-20 angiotensinogen Homo sapiens 37-43 14730203-7 2004 Ang II-enhanced intracellular ROS levels were inhibited by irbesartan and several antioxidants, and antioxidants also suppressed Ang II-induced ET-1 gene expression. Reactive Oxygen Species 30-33 angiotensinogen Homo sapiens 0-6 14730203-13 2004 CONCLUSIONS: Our data suggest that ROS are involved in Ang II-induced ET-1 gene expression within endothelial cells. Reactive Oxygen Species 35-38 angiotensinogen Homo sapiens 55-61 14769433-1 2004 One of the most prominent concepts to emerge in cardiovascular research over the past decade, especially in areas focused on angiotensin II (AngII), is that reactive oxygen species (ROS) are critical signaling molecules in a wide range of cellular processes. Reactive Oxygen Species 157-180 angiotensinogen Homo sapiens 125-139 14769433-1 2004 One of the most prominent concepts to emerge in cardiovascular research over the past decade, especially in areas focused on angiotensin II (AngII), is that reactive oxygen species (ROS) are critical signaling molecules in a wide range of cellular processes. Reactive Oxygen Species 157-180 angiotensinogen Homo sapiens 141-146 14769433-1 2004 One of the most prominent concepts to emerge in cardiovascular research over the past decade, especially in areas focused on angiotensin II (AngII), is that reactive oxygen species (ROS) are critical signaling molecules in a wide range of cellular processes. Reactive Oxygen Species 182-185 angiotensinogen Homo sapiens 125-139 14769433-1 2004 One of the most prominent concepts to emerge in cardiovascular research over the past decade, especially in areas focused on angiotensin II (AngII), is that reactive oxygen species (ROS) are critical signaling molecules in a wide range of cellular processes. Reactive Oxygen Species 182-185 angiotensinogen Homo sapiens 141-146 14769433-2 2004 Many of the physiological effects of AngII are mediated by ROS, and alterations in AngII-mediated redox mechanisms are implicated in cardiovascular diseases such as hypertension and atherosclerosis. Reactive Oxygen Species 59-62 angiotensinogen Homo sapiens 37-42 14769433-4 2004 Accumulating evidence suggests that ROS have important effects on central neural mechanisms involved in blood pressure regulation, volume homeostasis, and autonomic function, particularly those that involve AngII signaling. Reactive Oxygen Species 36-39 angiotensinogen Homo sapiens 207-212 14737835-6 2004 Angiotensin II and mechanical stress generate the reactive oxygen species through the activation of NADH/NADPH oxidase in hypertension. Reactive Oxygen Species 50-73 angiotensinogen Homo sapiens 0-14 14559857-11 2003 Both alkaloids inhibited Ang-II-induced endothelial P-selectin upregulation and the generation of reactive oxygen species (ROS) in endothelial cells stimulated with Ang-II, in fMLP-stimulated human neutrophils (PMNs) and in the hypoxanthine-xanthine oxidase system. Reactive Oxygen Species 98-121 angiotensinogen Homo sapiens 25-31 14559857-11 2003 Both alkaloids inhibited Ang-II-induced endothelial P-selectin upregulation and the generation of reactive oxygen species (ROS) in endothelial cells stimulated with Ang-II, in fMLP-stimulated human neutrophils (PMNs) and in the hypoxanthine-xanthine oxidase system. Reactive Oxygen Species 98-121 angiotensinogen Homo sapiens 165-171 14559857-11 2003 Both alkaloids inhibited Ang-II-induced endothelial P-selectin upregulation and the generation of reactive oxygen species (ROS) in endothelial cells stimulated with Ang-II, in fMLP-stimulated human neutrophils (PMNs) and in the hypoxanthine-xanthine oxidase system. Reactive Oxygen Species 123-126 angiotensinogen Homo sapiens 25-31 14559857-11 2003 Both alkaloids inhibited Ang-II-induced endothelial P-selectin upregulation and the generation of reactive oxygen species (ROS) in endothelial cells stimulated with Ang-II, in fMLP-stimulated human neutrophils (PMNs) and in the hypoxanthine-xanthine oxidase system. Reactive Oxygen Species 123-126 angiotensinogen Homo sapiens 165-171 14553961-14 2003 CONCLUSIONS: These data show that monocytes can be stimulated by AT(1)-AA and Ang II to adhere, produce tissue factor, and probably reactive oxygen species. Reactive Oxygen Species 132-155 angiotensinogen Homo sapiens 78-84 12970329-0 2003 Angiotensin II receptor blocker valsartan suppresses reactive oxygen species generation in leukocytes, nuclear factor-kappa B, in mononuclear cells of normal subjects: evidence of an antiinflammatory action. Reactive Oxygen Species 53-76 angiotensinogen Homo sapiens 0-14 12874098-4 2003 Activators of PPAR-alpha such as fatty acids and fibrates, and PPAR-gamma such as thiazolidinediones have been shown to exert antiproliferative effects, antagonize angiotensin II actions in vivo and in vitro, and exert antioxidant actions inhibiting generation of reactive oxygen species and activation of inflammatory mediators on blood vessels and the heart. Reactive Oxygen Species 264-287 angiotensinogen Homo sapiens 164-178 12860993-0 2003 Reactive oxygen species sensitivity of angiotensin II-dependent translation initiation in vascular smooth muscle cells. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 39-53 12860993-3 2003 Although angiotensin II (Ang II)-induced vascular smooth muscle cell hypertrophy requires the generation of reactive oxygen species (ROS), the ROS sensitivity of these events and their upstream activators remain unclear. Reactive Oxygen Species 108-131 angiotensinogen Homo sapiens 9-23 12860993-3 2003 Although angiotensin II (Ang II)-induced vascular smooth muscle cell hypertrophy requires the generation of reactive oxygen species (ROS), the ROS sensitivity of these events and their upstream activators remain unclear. Reactive Oxygen Species 108-131 angiotensinogen Homo sapiens 25-31 12860993-3 2003 Although angiotensin II (Ang II)-induced vascular smooth muscle cell hypertrophy requires the generation of reactive oxygen species (ROS), the ROS sensitivity of these events and their upstream activators remain unclear. Reactive Oxygen Species 133-136 angiotensinogen Homo sapiens 9-23 12860993-3 2003 Although angiotensin II (Ang II)-induced vascular smooth muscle cell hypertrophy requires the generation of reactive oxygen species (ROS), the ROS sensitivity of these events and their upstream activators remain unclear. Reactive Oxygen Species 133-136 angiotensinogen Homo sapiens 25-31 12860993-5 2003 Ang II-induced Ser-65 phosphorylation was ROS-dependent as assessed by pretreatment with ebselen (3.6 +/- 0.2 versus 1.1 +/- 0.2), diphenylene iodonium (3.6 +/- 0.2 versus 1.0 +/- 0.1), and N-acetyl cysteine (3.6 +/- 0.2 versus 1.2 +/- 0.1), but Ang II-stimulated phosphorylation of Thr-70 was ROS-insensitive. Reactive Oxygen Species 42-45 angiotensinogen Homo sapiens 0-6 12860993-5 2003 Ang II-induced Ser-65 phosphorylation was ROS-dependent as assessed by pretreatment with ebselen (3.6 +/- 0.2 versus 1.1 +/- 0.2), diphenylene iodonium (3.6 +/- 0.2 versus 1.0 +/- 0.1), and N-acetyl cysteine (3.6 +/- 0.2 versus 1.2 +/- 0.1), but Ang II-stimulated phosphorylation of Thr-70 was ROS-insensitive. Reactive Oxygen Species 42-45 angiotensinogen Homo sapiens 246-252 12860993-5 2003 Ang II-induced Ser-65 phosphorylation was ROS-dependent as assessed by pretreatment with ebselen (3.6 +/- 0.2 versus 1.1 +/- 0.2), diphenylene iodonium (3.6 +/- 0.2 versus 1.0 +/- 0.1), and N-acetyl cysteine (3.6 +/- 0.2 versus 1.2 +/- 0.1), but Ang II-stimulated phosphorylation of Thr-70 was ROS-insensitive. Reactive Oxygen Species 294-297 angiotensinogen Homo sapiens 0-6 12960680-3 2003 Furthermore, the authors investigated whether cerivastatin modulates an angiotensin II (10 micromol/L; 4 hours) induced reactive oxygen species (ROS) release from intact vessels (lucigenin-enhanced chemiluminescence-assay). Reactive Oxygen Species 120-143 angiotensinogen Homo sapiens 72-86 12960680-3 2003 Furthermore, the authors investigated whether cerivastatin modulates an angiotensin II (10 micromol/L; 4 hours) induced reactive oxygen species (ROS) release from intact vessels (lucigenin-enhanced chemiluminescence-assay). Reactive Oxygen Species 145-148 angiotensinogen Homo sapiens 72-86 12960680-7 2003 However, cerivastatin induced a significant concentration-dependent inhibition of the angiotensin II-induced ROS release from native endothelial cells of porcine coronary arteries. Reactive Oxygen Species 109-112 angiotensinogen Homo sapiens 86-100 12704649-7 2003 Thus, production of reactive oxygen species, aspirin (asp)-sensitive enzymes of the arachidonate metabolism, and NIK are common transducers of AII- and TNF-dependent pathways to NFkappaB. Reactive Oxygen Species 20-43 angiotensinogen Homo sapiens 143-146 12874439-7 2003 Advanced glycation end products, TGF-beta1, and angiotensin II can also induce ROS generation and may amplify high glucose-activated signaling in diabetic kidney. Reactive Oxygen Species 79-82 angiotensinogen Homo sapiens 48-62 12874440-3 2003 High glucose, advanced glycation end products, angiotensin II, and TGF-beta1 all increase intracellular reactive oxygen species (ROS) in renal cells and contribute to the development and progression of diabetic renal injury. Reactive Oxygen Species 104-127 angiotensinogen Homo sapiens 47-61 12874440-3 2003 High glucose, advanced glycation end products, angiotensin II, and TGF-beta1 all increase intracellular reactive oxygen species (ROS) in renal cells and contribute to the development and progression of diabetic renal injury. Reactive Oxygen Species 129-132 angiotensinogen Homo sapiens 47-61 12967772-4 2003 ROS produced following angiotensin II-mediated stimulation of NAD(P)H oxidases signal through pathways such as mitogen-activated protein kinases, tyrosine kinases and transcription factors, and lead to events such as inflammation, hypertrophy, remodeling and angiogenesis. Reactive Oxygen Species 0-3 angiotensinogen Homo sapiens 23-37 12897089-14 2003 CONCLUSIONS: The intracellular responses to Ang II mediated by reactive oxygen species are reduced in BS/GS patients. Reactive Oxygen Species 63-86 angiotensinogen Homo sapiens 44-50 12763763-6 2003 The generation of ROS by cultured HUVECs was significantly increased by angiotensin II. Reactive Oxygen Species 18-21 angiotensinogen Homo sapiens 72-86 12806586-2 2003 An important effect of Ang II is activation of the NAD(P)H oxidase, a major source of reactive oxygen species (ROS) production by vascular cells. Reactive Oxygen Species 86-109 angiotensinogen Homo sapiens 23-29 12806586-2 2003 An important effect of Ang II is activation of the NAD(P)H oxidase, a major source of reactive oxygen species (ROS) production by vascular cells. Reactive Oxygen Species 111-114 angiotensinogen Homo sapiens 23-29 12668498-5 2003 Angiotensin II (Ang II) and AT1-AA increased ROS production and the NADPH oxidase components, p22, p47, and p67 phox in Western blotting. Reactive Oxygen Species 45-48 angiotensinogen Homo sapiens 0-14 12560337-7 2003 Angiotensin II (100 nmol/liter)-induced reactive oxygen species production (as measured by dichlorohydrofluorescein fluorescence or lucigenin chemiluminescence) was completely absent in coronary microvascular endothelial cells isolated from p47(phox) knockout mice. Reactive Oxygen Species 40-63 angiotensinogen Homo sapiens 0-14 12668498-5 2003 Angiotensin II (Ang II) and AT1-AA increased ROS production and the NADPH oxidase components, p22, p47, and p67 phox in Western blotting. Reactive Oxygen Species 45-48 angiotensinogen Homo sapiens 16-22 12606520-7 2003 In addition, high glucose and angiotensin II promoted significantly increased generation of ROS in diabetic cardiomyocytes. Reactive Oxygen Species 92-95 angiotensinogen Homo sapiens 30-44 12606520-8 2003 Chronic overexpression of MT or acute in vitro treatment with the flavoprotein inhibitor diphenyleneiodonium or the angiotensin II type I receptor antagonist losartan eliminated excess ROS production in diabetic cardiomyocytes. Reactive Oxygen Species 185-188 angiotensinogen Homo sapiens 116-130 12606520-10 2003 Damage can be attributed to ROS production, and diabetes increases ROS production via angiotensin II and flavoprotein enzyme-dependent pathways. Reactive Oxygen Species 67-70 angiotensinogen Homo sapiens 86-100 12645638-5 2003 The signaling cascade for activation of the NAD(P)H oxidase by angiotensin II has recently been elucidated and seems to involve a feed-forward mechanism that permits ongoing production of ROS for prolonged periods. Reactive Oxygen Species 188-191 angiotensinogen Homo sapiens 63-77 12493759-4 2003 Treatment of vascular smooth muscle cells with angiotensin II as well as overexpression of the constitutively active mutant RacL61 increased ROS release as assessed by dichlorofluorescein fluorescence, whereas inhibition of Rac1 by Clostridium sordellii lethal toxin or overexpression of dominant-negative RacN17 inhibited ROS production. Reactive Oxygen Species 323-326 angiotensinogen Homo sapiens 47-61 12493759-4 2003 Treatment of vascular smooth muscle cells with angiotensin II as well as overexpression of the constitutively active mutant RacL61 increased ROS release as assessed by dichlorofluorescein fluorescence, whereas inhibition of Rac1 by Clostridium sordellii lethal toxin or overexpression of dominant-negative RacN17 inhibited ROS production. Reactive Oxygen Species 141-144 angiotensinogen Homo sapiens 47-61 12493759-5 2003 Treatment with E2 (100 nm) completely prevented angiotensin II-induced NAD(P)H oxidase activity and ROS production. Reactive Oxygen Species 100-103 angiotensinogen Homo sapiens 48-62 12573135-0 2002 Angiotensin II induces a rapid and transient increase of reactive oxygen species. Reactive Oxygen Species 57-80 angiotensinogen Homo sapiens 0-14 12379645-9 2002 These results establish that the non-hypoxic induction of the HIF-1 transcription factor via vasoactive hormones (Ang II and thrombin) is triggered by a dual mechanism, i.e. a PKC-mediated transcriptional action and a ROS-dependent increase in HIF-1alpha protein expression. Reactive Oxygen Species 218-221 angiotensinogen Homo sapiens 114-120 12573139-0 2002 NAD(P)H oxidase-derived reactive oxygen species as mediators of angiotensin II signaling. Reactive Oxygen Species 24-47 angiotensinogen Homo sapiens 64-78 12573139-3 2002 Angiotensin II has been shown to activate the vascular NAD(P)H oxidase(s) resulting in the production of reactive oxygen species, namely superoxide and hydrogen peroxide. Reactive Oxygen Species 105-128 angiotensinogen Homo sapiens 0-14 12171785-5 2002 Recent work has shown that angiotensin II (Ang II) has significant proinflammatory actions in the vascular wall, inducing the production of reactive oxygen species, inflammatory cytokines, and adhesion molecules. Reactive Oxygen Species 140-163 angiotensinogen Homo sapiens 27-41 12573139-4 2002 In this article, we review what is known about the molecular steps that link angiotensin II and its receptor to production of reactive oxygen species and subsequent redox-mediated events, focusing on the structural and functional properties of the vascular NAD(P)H oxidases and their downstream mediators. Reactive Oxygen Species 126-149 angiotensinogen Homo sapiens 77-91 12397680-1 2002 Angiotensin II(AngII) activates NADH/NAPDH oxidase activity and stimulates reactive oxygen species(ROS) production, which induces many proinflammatory genes such as vascular cell adhesion molecule-1(VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and monocyte chemoattractant protein-1(MCP-1) mainly via AngII type I receptor(AT1). Reactive Oxygen Species 99-102 angiotensinogen Homo sapiens 0-14 12383592-4 2002 Angiotensin II stimulates nicotinamide adenine dinucleotide phosphate (NADPH)/nicotinamide adenine dinucleotide (NADH) oxidase in endothelium, smooth muscle cells, and the adventitia of blood vessels to generate reactive oxygen species, leading to endothelial dysfunction, growth, and inflammation. Reactive Oxygen Species 212-235 angiotensinogen Homo sapiens 0-14 12397680-1 2002 Angiotensin II(AngII) activates NADH/NAPDH oxidase activity and stimulates reactive oxygen species(ROS) production, which induces many proinflammatory genes such as vascular cell adhesion molecule-1(VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and monocyte chemoattractant protein-1(MCP-1) mainly via AngII type I receptor(AT1). Reactive Oxygen Species 75-98 angiotensinogen Homo sapiens 0-14 12171785-5 2002 Recent work has shown that angiotensin II (Ang II) has significant proinflammatory actions in the vascular wall, inducing the production of reactive oxygen species, inflammatory cytokines, and adhesion molecules. Reactive Oxygen Species 140-163 angiotensinogen Homo sapiens 43-49 11597988-11 2001 Ang II phosphorylated CREB through the ERK and p38 MAPK pathway in a ROS-sensitive manner. Reactive Oxygen Species 69-72 angiotensinogen Homo sapiens 0-6 12036387-2 2002 A single unifying mechanism of increased production of reactive oxygen species (ROS) by angiotensin II (Ang II) may serve as a causal link between hyperglycaemia and hypercholesterolaemia and many of the major pathways responsible for atherogenic and diabetic disorders. Reactive Oxygen Species 55-78 angiotensinogen Homo sapiens 88-102 12036387-2 2002 A single unifying mechanism of increased production of reactive oxygen species (ROS) by angiotensin II (Ang II) may serve as a causal link between hyperglycaemia and hypercholesterolaemia and many of the major pathways responsible for atherogenic and diabetic disorders. Reactive Oxygen Species 55-78 angiotensinogen Homo sapiens 104-110 12036387-2 2002 A single unifying mechanism of increased production of reactive oxygen species (ROS) by angiotensin II (Ang II) may serve as a causal link between hyperglycaemia and hypercholesterolaemia and many of the major pathways responsible for atherogenic and diabetic disorders. Reactive Oxygen Species 80-83 angiotensinogen Homo sapiens 88-102 12036387-2 2002 A single unifying mechanism of increased production of reactive oxygen species (ROS) by angiotensin II (Ang II) may serve as a causal link between hyperglycaemia and hypercholesterolaemia and many of the major pathways responsible for atherogenic and diabetic disorders. Reactive Oxygen Species 80-83 angiotensinogen Homo sapiens 104-110 11597988-0 2001 ERK and p38 MAPK, but not NF-kappaB, are critically involved in reactive oxygen species-mediated induction of IL-6 by angiotensin II in cardiac fibroblasts. Reactive Oxygen Species 64-87 angiotensinogen Homo sapiens 118-132 11597988-3 2001 Ang II increased intracellular ROS in cardiac fibroblasts, and the increase was completely inhibited by the AT-1 blocker candesartan and the NADH/NADPH oxidase inhibitor diphenyleneiodonium (DPI). Reactive Oxygen Species 31-34 angiotensinogen Homo sapiens 0-6 11597988-12 2001 Collectively, these data indicated that Ang II stimulated ROS production via the AT1 receptor and NADH/NADPH oxidase, and that these ROS mediated activation of MAPKs, which culminated in IL-6 gene expression through a CRE-dependent, but not NF-kappaB-dependent, pathway in cardiac fibroblasts. Reactive Oxygen Species 58-61 angiotensinogen Homo sapiens 40-46 11597988-12 2001 Collectively, these data indicated that Ang II stimulated ROS production via the AT1 receptor and NADH/NADPH oxidase, and that these ROS mediated activation of MAPKs, which culminated in IL-6 gene expression through a CRE-dependent, but not NF-kappaB-dependent, pathway in cardiac fibroblasts. Reactive Oxygen Species 133-136 angiotensinogen Homo sapiens 40-46 11446714-7 2001 Ang II-induced generation of DPI-inhibitable ROS was significantly enhanced in cells from hypertensives compared with normotensives (Emax = 72 +/- 2 versus 56.9 +/- 1.8 fluorescence units, P< 0.01). Reactive Oxygen Species 45-48 angiotensinogen Homo sapiens 0-6 11446714-8 2001 PLD inhibition attenuated Ang II-induced ROS generation, with greater effects in the hypertensive group than the normotensive group (delta = 42 +/- 3.3 versus 21 +/- 2 units). Reactive Oxygen Species 41-44 angiotensinogen Homo sapiens 26-32 11334765-3 2001 In vascular cells, Ang II is a potent stimulus for the generation of reactive oxygen species. Reactive Oxygen Species 69-92 angiotensinogen Homo sapiens 19-25 11304462-0 2001 Epidermal growth factor receptor transactivation by angiotensin II requires reactive oxygen species in vascular smooth muscle cells. Reactive Oxygen Species 76-99 angiotensinogen Homo sapiens 52-66 11304462-4 2001 Here, we provide novel evidence that ROS are critical mediators of EGF-R transactivation by Ang II. Reactive Oxygen Species 37-40 angiotensinogen Homo sapiens 92-98 11304462-10 2001 These findings emphasize the importance of ROS in specific Ang II-stimulated growth-related signaling pathways and suggest that redox-sensitive EGF-R transactivation may be a potential target for antioxidant therapy in vascular disease. Reactive Oxygen Species 43-46 angiotensinogen Homo sapiens 59-65 11162642-5 2001 These data indicate that ROS mediate Ang II-induced EGF receptor transactivation, a critical mechanism for ERK-dependent growth in VSMCs. Reactive Oxygen Species 25-28 angiotensinogen Homo sapiens 37-43 11162642-1 2001 Angiotensin II (Ang II) is known to stimulate reactive oxygen species (ROS) generation and epidermal growth factor (EGF) receptor transactivation to mediate growth-promoting signals such as extracellular signal-regulated kinase (ERK) in vascular smooth muscle cells (VSMCs). Reactive Oxygen Species 46-69 angiotensinogen Homo sapiens 0-14 10428852-0 1999 Reactive oxygen species mediate the activation of Akt/protein kinase B by angiotensin II in vascular smooth muscle cells. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 74-88 11162642-1 2001 Angiotensin II (Ang II) is known to stimulate reactive oxygen species (ROS) generation and epidermal growth factor (EGF) receptor transactivation to mediate growth-promoting signals such as extracellular signal-regulated kinase (ERK) in vascular smooth muscle cells (VSMCs). Reactive Oxygen Species 46-69 angiotensinogen Homo sapiens 16-22 11162642-1 2001 Angiotensin II (Ang II) is known to stimulate reactive oxygen species (ROS) generation and epidermal growth factor (EGF) receptor transactivation to mediate growth-promoting signals such as extracellular signal-regulated kinase (ERK) in vascular smooth muscle cells (VSMCs). Reactive Oxygen Species 71-74 angiotensinogen Homo sapiens 0-14 11162642-1 2001 Angiotensin II (Ang II) is known to stimulate reactive oxygen species (ROS) generation and epidermal growth factor (EGF) receptor transactivation to mediate growth-promoting signals such as extracellular signal-regulated kinase (ERK) in vascular smooth muscle cells (VSMCs). Reactive Oxygen Species 71-74 angiotensinogen Homo sapiens 16-22 11023939-10 2000 Angiotensin II-induced release of reactive oxygen species was inhibited by estrogens. Reactive Oxygen Species 34-57 angiotensinogen Homo sapiens 0-14 10965882-0 2000 Involvement of reactive oxygen species in the activation of tyrosine kinase and extracellular signal-regulated kinase by angiotensin II. Reactive Oxygen Species 15-38 angiotensinogen Homo sapiens 121-135 10965882-1 2000 Reactive oxygen species (ROS) have been proposed to mediate vascular hypertrophy induced by angiotensin II (Ang II). Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 92-106 10965882-1 2000 Reactive oxygen species (ROS) have been proposed to mediate vascular hypertrophy induced by angiotensin II (Ang II). Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 108-114 10965882-1 2000 Reactive oxygen species (ROS) have been proposed to mediate vascular hypertrophy induced by angiotensin II (Ang II). Reactive Oxygen Species 25-28 angiotensinogen Homo sapiens 92-106 10965882-1 2000 Reactive oxygen species (ROS) have been proposed to mediate vascular hypertrophy induced by angiotensin II (Ang II). Reactive Oxygen Species 25-28 angiotensinogen Homo sapiens 108-114 10965882-3 2000 However, whether ROS contribute to the Ang II-induced PTK and/or ERK activation in vascular smooth muscle cells (VSMCs) remains largely unclear. Reactive Oxygen Species 17-20 angiotensinogen Homo sapiens 39-45 10965882-4 2000 Here, we have investigated the possible involvement of ROS in Ang II-induced PTK and ERK activation. Reactive Oxygen Species 55-58 angiotensinogen Homo sapiens 62-68 10965882-9 2000 From these data, we conclude that ROS play a critical role in the Ang II-induced PTK and ERK activation in VSMCs, thereby contributing to vascular growth associated with enhanced Ang II activity. Reactive Oxygen Species 34-37 angiotensinogen Homo sapiens 66-72 10965882-9 2000 From these data, we conclude that ROS play a critical role in the Ang II-induced PTK and ERK activation in VSMCs, thereby contributing to vascular growth associated with enhanced Ang II activity. Reactive Oxygen Species 34-37 angiotensinogen Homo sapiens 179-185 10837481-8 2000 Finally, strong induction of VEGF mRNA by Ang II can also be inhibited by these ROS inhibitors. Reactive Oxygen Species 80-83 angiotensinogen Homo sapiens 42-48 10906152-0 2000 Reactive oxygen species stimulate p44/42 mitogen-activated protein kinase and induce p27(Kip1): role in angiotensin II-mediated hypertrophy of proximal tubular cells. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 104-118 10906152-8 2000 The flavoprotein inhibitor diphenylene iodinium, as well as the antioxidant N-acetylcysteine, prevented AngII-induced p44/42 MAP kinase phosphorylation, indicating involvement of reactive oxygen species generated by membrane-bound NAD(P)H oxidase. Reactive Oxygen Species 179-202 angiotensinogen Homo sapiens 104-109 11862018-5 2001 Angiotensin II enhances the formation of reactive oxygen species via the activation of xanthine oxidase or NAD(P)H oxidase. Reactive Oxygen Species 41-64 angiotensinogen Homo sapiens 0-14 10967199-0 2000 Reactive oxygen species as mediators of angiotensin II signaling. Reactive Oxygen Species 0-23 angiotensinogen Homo sapiens 40-54 10967199-2 2000 Recent work has shown that reactive oxygen species are involved in transducing many of the effects of angiotensin II, and are in fact produced in response to agonist-receptor binding. Reactive Oxygen Species 27-50 angiotensinogen Homo sapiens 102-116 10981145-2 2000 Recent studies provide evidence that ANG II could stimulate intracellular formation of reactive oxygen species (ROS) such as the superoxide anion (O2-). Reactive Oxygen Species 87-110 angiotensinogen Homo sapiens 37-43 10981145-2 2000 Recent studies provide evidence that ANG II could stimulate intracellular formation of reactive oxygen species (ROS) such as the superoxide anion (O2-). Reactive Oxygen Species 112-115 angiotensinogen Homo sapiens 37-43 10981145-3 2000 This ANG II-mediated ROS formation exhibits different kinetic and lower absolute concentrations than those traditionally observed during the respiratory burst of phagocytic cells, but it likely involves similar membrane-bound NAD(P)H-oxidases. Reactive Oxygen Species 21-24 angiotensinogen Homo sapiens 5-11 10981145-6 2000 ANG II-induced ROS play a pivotal role in several pathophysiologic situations of vascular and renal cells such as hypertension, endothelial dysfunction, nitrate tolerance, atherosclerosis, and cellular remodeling. Reactive Oxygen Species 15-18 angiotensinogen Homo sapiens 0-6 10428852-8 1999 Thus, our studies indicate that Akt/PKB is part of the remarkable spectrum of angiotensin II signaling pathways and provide insight into the highly organized signaling mechanisms coordinated by ROS, which mediate the hypertrophic response to angiotensin II in VSMCs. Reactive Oxygen Species 194-197 angiotensinogen Homo sapiens 242-256 10428852-1 1999 Angiotensin II, a hypertrophic/anti-apoptotic hormone, utilizes reactive oxygen species (ROS) as growth-related signaling molecules in vascular smooth muscle cells (VSMCs). Reactive Oxygen Species 64-87 angiotensinogen Homo sapiens 0-14 10428852-1 1999 Angiotensin II, a hypertrophic/anti-apoptotic hormone, utilizes reactive oxygen species (ROS) as growth-related signaling molecules in vascular smooth muscle cells (VSMCs). Reactive Oxygen Species 89-92 angiotensinogen Homo sapiens 0-14 10428852-6 1999 Furthermore, diphenylene iodonium, an inhibitor of flavin-containing oxidases, or overexpression of catalase to block angiotensin II-induced intracellular H(2)O(2) production significantly inhibits angiotensin II-induced Akt/PKB phosphorylation, indicating a role for ROS in agonist-induced Akt/PKB activation. Reactive Oxygen Species 268-271 angiotensinogen Homo sapiens 118-132 10428852-6 1999 Furthermore, diphenylene iodonium, an inhibitor of flavin-containing oxidases, or overexpression of catalase to block angiotensin II-induced intracellular H(2)O(2) production significantly inhibits angiotensin II-induced Akt/PKB phosphorylation, indicating a role for ROS in agonist-induced Akt/PKB activation. Reactive Oxygen Species 268-271 angiotensinogen Homo sapiens 198-212 34836751-4 2022 Patients with such comorbidities exhibit elevated levels of reactive oxygen species (ROS) and oxidative stress caused by an increased accumulation of angiotensin II and by activation of the NADPH oxidase pathway. Reactive Oxygen Species 60-83 angiotensinogen Homo sapiens 150-164 10069678-0 1999 Acute simultaneous stimulation of nitric oxide and oxygen radicals by angiotensin II in humans in vivo. Reactive Oxygen Species 51-66 angiotensinogen Homo sapiens 70-84 10069678-8 1999 In conclusion, this study demonstrates that the constrictor actions of angiotensin II are enhanced during NO clamp and attenuated during vitamin C, suggesting direct angiotensin II-associated stimulation of endothelial NO and of oxygen radicals, respectively, in humans in vivo. Reactive Oxygen Species 229-244 angiotensinogen Homo sapiens 71-85 10069678-8 1999 In conclusion, this study demonstrates that the constrictor actions of angiotensin II are enhanced during NO clamp and attenuated during vitamin C, suggesting direct angiotensin II-associated stimulation of endothelial NO and of oxygen radicals, respectively, in humans in vivo. Reactive Oxygen Species 229-244 angiotensinogen Homo sapiens 166-180 7573383-2 1995 Because angiotensin II (ANG II) contracts arterial smooth muscle by mobilizing intracellular Ca2+ concentrations ([Ca2+])i, we determined the effects of ROS pretreatment on ANG II-induced contractions in coronary artery rings and [Ca2+]i transients in smooth muscle cells (SMC) cultured from them. Reactive Oxygen Species 153-156 angiotensinogen Homo sapiens 173-179 34783022-2 2022 In this study, we evaluated whether the inhibition of class I HDACs can attenuate angiotensin II (ANG II)-induced fibrogenesis and mitochondrial malfunction through its effects on reactive oxygen species (ROS) and calcium dysregulation in human cardiac fibroblasts (CFs). Reactive Oxygen Species 180-203 angiotensinogen Homo sapiens 82-96 34783022-2 2022 In this study, we evaluated whether the inhibition of class I HDACs can attenuate angiotensin II (ANG II)-induced fibrogenesis and mitochondrial malfunction through its effects on reactive oxygen species (ROS) and calcium dysregulation in human cardiac fibroblasts (CFs). Reactive Oxygen Species 180-203 angiotensinogen Homo sapiens 98-104 34783022-2 2022 In this study, we evaluated whether the inhibition of class I HDACs can attenuate angiotensin II (ANG II)-induced fibrogenesis and mitochondrial malfunction through its effects on reactive oxygen species (ROS) and calcium dysregulation in human cardiac fibroblasts (CFs). Reactive Oxygen Species 205-208 angiotensinogen Homo sapiens 82-96 34783022-2 2022 In this study, we evaluated whether the inhibition of class I HDACs can attenuate angiotensin II (ANG II)-induced fibrogenesis and mitochondrial malfunction through its effects on reactive oxygen species (ROS) and calcium dysregulation in human cardiac fibroblasts (CFs). Reactive Oxygen Species 205-208 angiotensinogen Homo sapiens 98-104 10397679-11 1999 Pyrrolidine dithiocarbamate suppressed angiotensin II-induced IL-6 release, a finding compatible with involvement of reactive oxygen species as second messengers in cytokine production mediated by angiotensin. Reactive Oxygen Species 117-140 angiotensinogen Homo sapiens 39-53 9885178-3 1998 ROS formation can be stimulated by mechanical stress, environmental factors, the peptide angiotensin II, cytokines, native low-density lipoproteins (LDL), and in the presence of catalytic metal ions. Reactive Oxygen Species 0-3 angiotensinogen Homo sapiens 89-103 34864165-5 2022 We found that angiotensin II-treated atria exhibited significantly elevated BCAA level, reduced BCAA catabolic enzyme activity, increased AF vulnerability, aggravated atrial electrical and structural remodeling, and enhanced mitochondrial ROS damage. Reactive Oxygen Species 239-242 angiotensinogen Homo sapiens 14-28 34783022-4 2022 Compared with controls, ANG II-treated CFs had greater migration activity, higher ATP production, maximal respiration, and spare capacity with higher mitochondrial Ca2+ uptake and ROS generation, which was attenuated by the administration of MS-275. Reactive Oxygen Species 180-183 angiotensinogen Homo sapiens 24-30 34836751-4 2022 Patients with such comorbidities exhibit elevated levels of reactive oxygen species (ROS) and oxidative stress caused by an increased accumulation of angiotensin II and by activation of the NADPH oxidase pathway. Reactive Oxygen Species 85-88 angiotensinogen Homo sapiens 150-164 34453839-8 2021 Our data further show that nebivolol and nebivolol/valsartan combination mediated up-regulation in mitochondrial biogenesis is accompanied by decrease in ANG II-stimulated mitochondrial ROS generation as well as increase in expression of mitochondrial fusion genes MFN2 and OPA1, indicative of improved mitochondrial dynamics. Reactive Oxygen Species 186-189 angiotensinogen Homo sapiens 154-160 34486189-5 2021 We employed an immortalized endothelial cell line (bEnd.3) to mimic a BBB monolayer model in vitro and investigated the effect of harpagoside on BBB and found that harpagoside alleviated Ang II-induced BBB destruction, inhibited Ang II-associated cytotoxicity in a concentration-dependent manner and attenuated Ang II-induced reactive oxygen species (ROS) impair by downregulation of Nox2, Nox4, and COX-2. Reactive Oxygen Species 326-349 angiotensinogen Homo sapiens 311-317 34486189-5 2021 We employed an immortalized endothelial cell line (bEnd.3) to mimic a BBB monolayer model in vitro and investigated the effect of harpagoside on BBB and found that harpagoside alleviated Ang II-induced BBB destruction, inhibited Ang II-associated cytotoxicity in a concentration-dependent manner and attenuated Ang II-induced reactive oxygen species (ROS) impair by downregulation of Nox2, Nox4, and COX-2. Reactive Oxygen Species 351-354 angiotensinogen Homo sapiens 311-317 34829520-6 2021 In this review, we highlight recent advances regarding the regulation of NRF2, including the effect of Angiotensin II as an endogenous signalling molecule able to regulate ROS production and oxidative stress in dopaminergic neurons. Reactive Oxygen Species 172-175 angiotensinogen Homo sapiens 103-117 34324440-8 2021 Ang II induced NETosis in vitro via a reactive oxygen species (ROS)/peptidylarginine deiminase type 4 and autophagy-dependent pathway. Reactive Oxygen Species 38-61 angiotensinogen Homo sapiens 0-6 34324440-8 2021 Ang II induced NETosis in vitro via a reactive oxygen species (ROS)/peptidylarginine deiminase type 4 and autophagy-dependent pathway. Reactive Oxygen Species 63-66 angiotensinogen Homo sapiens 0-6 34285710-7 2021 Results: (1) Cell size decreased significantly in Ang II-treated cells; (2) MAP2 and ROS increased significantly in Ang II-treated cells with no changes in viability; (3) MAP2 and ROS decreased significantly in cells incubated with Ang II plus apocynin. Reactive Oxygen Species 85-88 angiotensinogen Homo sapiens 116-122 34132029-9 2021 Angiotensin II (Ang II) induced VSMC senescence by promoting ROS generation. Reactive Oxygen Species 61-64 angiotensinogen Homo sapiens 0-14 34132029-9 2021 Angiotensin II (Ang II) induced VSMC senescence by promoting ROS generation. Reactive Oxygen Species 61-64 angiotensinogen Homo sapiens 16-22 34132029-11 2021 Mechanistically, Ang II treatment significantly elevated miR-199a-5p level, thereby stimulating ROS generation by repressing Sirt1 and consequent VSMC senescence. Reactive Oxygen Species 96-99 angiotensinogen Homo sapiens 17-23 34285710-0 2021 Angiotensin II Induces Differentiation of Human Neuroblastoma Cells by Increasing MAP2 and ROS Levels. Reactive Oxygen Species 91-94 angiotensinogen Homo sapiens 0-14 34285710-2 2021 In this study, we investigated if Ang II influences differentiation of human neuroblastoma cells with simultaneous activation of NADPH oxidase and reactive oxygen species (ROS). Reactive Oxygen Species 147-170 angiotensinogen Homo sapiens 34-40 34285710-7 2021 Results: (1) Cell size decreased significantly in Ang II-treated cells; (2) MAP2 and ROS increased significantly in Ang II-treated cells with no changes in viability; (3) MAP2 and ROS decreased significantly in cells incubated with Ang II plus apocynin. Reactive Oxygen Species 85-88 angiotensinogen Homo sapiens 232-238 34285710-7 2021 Results: (1) Cell size decreased significantly in Ang II-treated cells; (2) MAP2 and ROS increased significantly in Ang II-treated cells with no changes in viability; (3) MAP2 and ROS decreased significantly in cells incubated with Ang II plus apocynin. Reactive Oxygen Species 85-88 angiotensinogen Homo sapiens 50-56 34285710-7 2021 Results: (1) Cell size decreased significantly in Ang II-treated cells; (2) MAP2 and ROS increased significantly in Ang II-treated cells with no changes in viability; (3) MAP2 and ROS decreased significantly in cells incubated with Ang II plus apocynin. Reactive Oxygen Species 180-183 angiotensinogen Homo sapiens 50-56 34285710-7 2021 Results: (1) Cell size decreased significantly in Ang II-treated cells; (2) MAP2 and ROS increased significantly in Ang II-treated cells with no changes in viability; (3) MAP2 and ROS decreased significantly in cells incubated with Ang II plus apocynin. Reactive Oxygen Species 180-183 angiotensinogen Homo sapiens 116-122 34285710-7 2021 Results: (1) Cell size decreased significantly in Ang II-treated cells; (2) MAP2 and ROS increased significantly in Ang II-treated cells with no changes in viability; (3) MAP2 and ROS decreased significantly in cells incubated with Ang II plus apocynin. Reactive Oxygen Species 180-183 angiotensinogen Homo sapiens 232-238 34208136-2 2021 SARS-CoV-2 infection occurs through the interaction of the viral protein Spike with the angiotensin II receptor (ACE 2), leading to an increase of angiotensin II and activation of nicotinamide adenine dinucleotide phosphate oxidase2 (NOX2), resulting in the release of both reactive oxygen species (ROS) and inflammatory molecules. Reactive Oxygen Species 274-297 angiotensinogen Homo sapiens 147-161 34208136-2 2021 SARS-CoV-2 infection occurs through the interaction of the viral protein Spike with the angiotensin II receptor (ACE 2), leading to an increase of angiotensin II and activation of nicotinamide adenine dinucleotide phosphate oxidase2 (NOX2), resulting in the release of both reactive oxygen species (ROS) and inflammatory molecules. Reactive Oxygen Species 299-302 angiotensinogen Homo sapiens 147-161 35453328-0 2022 Ginsenoside Rh1 Inhibits Angiotensin II-Induced Vascular Smooth Muscle Cell Migration and Proliferation through Suppression of the ROS-Mediated ERK1/2/p90RSK/KLF4 Signaling Pathway. Reactive Oxygen Species 131-134 angiotensinogen Homo sapiens 25-39