PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19427495-2 2009 There is evidence that hypertensive stimuli, such as high salt and angiotensin II, promote the production of ROS in the brain, the kidney, and the vasculature and that each of these sites contributes either to hypertension or to the untoward sequelae of this disease. ros 109-112 angiotensinogen Homo sapiens 67-81 17262974-0 2006 [Mechanisms of ROS induced by angiotensin II and its roles in vascular damage]. ros 15-18 angiotensinogen Homo sapiens 30-44 19161983-2 2009 Here, we report that Ang II-induced MC apoptosis in a time-dependent manner and up-regulated TLR4/MyD88 expression, and that the intracellular ROS was subsequently increased. ros 143-146 angiotensinogen Homo sapiens 21-27 18495130-3 2009 Angiotensin II in addition to stimulating vasoconstriction also induces an increase in ROS and a proinflammatory phenotype via AT(1)R. ros 87-90 angiotensinogen Homo sapiens 0-14 18467643-4 2008 Nox4 overexpression substantially increased basal ROS generation whereas ROS generation in response to angiotensin II and tumor necrosis factor (TNF)alpha was enhanced in Nox2-overexpressing cells. ros 73-76 angiotensinogen Homo sapiens 103-143 12663441-5 2003 Furthermore, Ang II induced a robust phosphorylation of p38MAPK, ERK1/2, and JNK1/2 (particularly JNK2), which was hindered by inhibitors of NADPH oxidase, tyrosine kinases, and ROS scavengers. ros 178-181 angiotensinogen Homo sapiens 13-19 12663441-7 2003 Present data demonstrate for the first time a stimulatory role of Ang II in the activation of phagocytic cells, underscore the relevant role of ROS as mediators in this process, and uncover a variety of signaling pathways by which Ang II operates in human neutrophils. ros 144-147 angiotensinogen Homo sapiens 66-72 12663441-7 2003 Present data demonstrate for the first time a stimulatory role of Ang II in the activation of phagocytic cells, underscore the relevant role of ROS as mediators in this process, and uncover a variety of signaling pathways by which Ang II operates in human neutrophils. ros 144-147 angiotensinogen Homo sapiens 231-237 35218740-10 2022 Taken together, the present study indicates that CORM-2-induced Nrf2/HO-1 alleviates IL-6/Jak2/Stat3-mediated inflammatory responses to Ang II by inhibiting NADPH oxidase- and mitochondria-derived ROS, suggesting that CORM-2 is a promising pharmacologic candidate to reverse the pathological changes involved in the inflammation of vessel wall for the prevention and treatment of AAA. ros 197-200 angiotensinogen Homo sapiens 136-142 33773140-0 2021 Asenapine maleate inhibits angiotensin II-induced proliferation and activation of cardiac fibroblasts via the ROS/TGFbeta1/MAPK signaling pathway. ros 110-113 angiotensinogen Homo sapiens 27-41 34206708-9 2021 Importantly, while stimulating the production of ROS, Angiotensin-II at the same time decreases the generation of NO. ros 49-52 angiotensinogen Homo sapiens 54-68 35218740-0 2022 Carbon monoxide releasing molecule-2 attenuates angiotensin II-induced IL-6/Jak2/Stat3-associated inflammation by inhibiting NADPH oxidase- and mitochondria-derived ROS in human aortic smooth muscle cells. ros 165-168 angiotensinogen Homo sapiens 48-62 35218740-2 2022 Angiotensin II (Ang II) involves in AAA progression by promoting the proliferation and migration of vascular smooth muscle cells, the degradation of extracellular matrices, and the generation of ROS to lead to vascular inflammation. ros 195-198 angiotensinogen Homo sapiens 0-14 35218740-2 2022 Angiotensin II (Ang II) involves in AAA progression by promoting the proliferation and migration of vascular smooth muscle cells, the degradation of extracellular matrices, and the generation of ROS to lead to vascular inflammation. ros 195-198 angiotensinogen Homo sapiens 16-22 30262241-0 2020 Corrigendum to "CO-releasing molecules CORM2 attenuates angiotensin II-induced human aortic smooth muscle cell migration through inhibition of ROS/IL-6 generation and matrix metalloproteinases-9 expression" [Redox Biol. ros 143-146 angiotensinogen Homo sapiens 56-70 35218740-6 2022 The results showed that Ang II induced inflammatory responses of HASMCs via NADPH oxidase- and mitochondria-derived ROS/NF-kappaB/IL-6/Jak2/Stat3 pathway which was attenuated by the pretreatment with CORM-2. ros 116-119 angiotensinogen Homo sapiens 24-30 32977573-10 2020 Moreover, pretreatment of sauchinone inhibited NF-kappaB translocation and ROS production in AngII-exposed mesangial cells. ros 75-78 angiotensinogen Homo sapiens 93-98 33239867-10 2020 Loxoprofen ameliorated Angiotensin II-induced production of ROS, reduced GSH, and NOX-2 and NOX-4 expression. ros 60-63 angiotensinogen Homo sapiens 23-37 33226363-6 2020 AngII decreased cell viability and PRDX6, upregulated the expression levels of TNF-alpha, IL-6, IL-1beta, LDH and MDA, stimulated ROS production, and reduced NO synthase, the expressions of eNOS, MnSOD, ICAM-1, VCAM-1, and activated the MAPK family of signaling proteins. ros 130-133 angiotensinogen Homo sapiens 0-5 32592919-8 2020 It is known that the activation of endothelial estrogen receptors increases NO and decreases ROS, protecting the vascular system from angiotensin II-mediated vasoconstriction, inflammation, and ROS production. ros 93-96 angiotensinogen Homo sapiens 134-148 31390228-0 2019 Angiotensin II deteriorates advanced atherosclerosis by promoting MerTK cleavage and impairing efferocytosis through AT1R/ROS/p38MAPK/ADAM17 pathway. ros 122-125 angiotensinogen Homo sapiens 0-14 31390228-5 2019 Ang II-activated ADAM17 required ROS and p38 MAPK phosphorylation. ros 33-36 angiotensinogen Homo sapiens 0-6 31084929-7 2019 Furthermore, we found that superoxide anion levels were significantly increased in AngII-treated endothelial cells compared with controls and that the ROS scavenger N-acetyl-l-cysteine (NAC) significantly abolished CSE ubiquitination. ros 151-154 angiotensinogen Homo sapiens 83-88 31390228-12 2019 In conclusion, Ang II promotes MerTK shedding via AT1R/ROS/p38MAPK/ADAM17 pathway in macrophages, which led to defective efferocytosis and atherosclerosis progression. ros 55-58 angiotensinogen Homo sapiens 15-21 31084929-0 2019 Angiotensin II downregulates vascular endothelial cell hydrogen sulfide production by enhancing cystathionine gamma-lyase degradation through ROS-activated ubiquitination pathway. ros 142-145 angiotensinogen Homo sapiens 0-14 31084929-8 2019 Taken together, our data suggested that AngII inhibited endogenous H2S generation through ubiquitination-mediated CSE degradation via the ROS pathway in vascular endothelial cells. ros 138-141 angiotensinogen Homo sapiens 40-45 30928096-6 2019 Here, we found that H2 relaxin increased eNOS, SOD1 expression, inhibited excessive mitochondrial fission and decreased ROS level in HUVECs treated with AngII. ros 120-123 angiotensinogen Homo sapiens 153-158 30928096-7 2019 However, overexpression of fission protein 1 (Fis1) prevented H2 relaxin from protecting against AngII-induced low eNOS, SOD1 expression, excessive mitochondrial fission and increased ROS level in HUVECs. ros 184-187 angiotensinogen Homo sapiens 97-102 30914692-6 2019 Ang II-induced elevated intracellular ROS levels were detected only when the cells were pre-incubated with high levels of glucose (13.5 mM, 27.8 mM), but was not detected under normal glucose condition (5.5 mM). ros 38-41 angiotensinogen Homo sapiens 0-6 30914692-10 2019 In conclusion, Ang II-induced oxidative stress was augmented by high glucose levels and ROS levels were further alleviated in the presence of AT1R antagonists. ros 88-91 angiotensinogen Homo sapiens 15-21 30914692-7 2019 Production of Ang II-induced intracellular ROS was higher under pre-treatment with 27.8 mM glucose compared to pretreatment with 13.5 mM glucose level. ros 43-46 angiotensinogen Homo sapiens 14-20 30914692-8 2019 This ROS production in mesangial cells was induced within several minutes of the initiation of Ang II stimulation under high glucose levels. ros 5-8 angiotensinogen Homo sapiens 95-101 30662355-6 2019 Moreover, SFN reduced the Ang II-induced upregulation of HVSMC migration; this effect was inhibited by pretreatment with inhibitors of NADPH oxidase and ROS or transfection with siNOX4. ros 153-156 angiotensinogen Homo sapiens 26-32 29272019-5 2017 RESULTS: Our study found that ARRB2 could significantly reduce the generation and release of ROS, endothelin-1 (ET-1), lactic dehydrogenase (LDH) of HUVECs induced by Ang II and promote the generation of NO, superoxide dismutase (SOD) and scavenging in a dose-dependent manner. ros 93-96 angiotensinogen Homo sapiens 167-173 27565029-11 2016 Moreover, AngII and miR-106a treatment cultured cardiomyocytes mitochondria presented cristae defects, considerable depolarization of mitochondrial membrane and increased ROS production. ros 171-174 angiotensinogen Homo sapiens 10-15 28292711-0 2017 CO-releasing molecules CORM2 attenuates angiotensin II-induced human aortic smooth muscle cell migration through inhibition of ROS/IL-6 generation and matrix metalloproteinases-9 expression. ros 127-130 angiotensinogen Homo sapiens 40-54 23054367-7 2013 Conversely, ethanol-induced ROS generation was inhibited if VDR was activated or Ang II was blocked by an angiotensin II type 1 (AT1) receptor blocker (Losartan). ros 28-31 angiotensinogen Homo sapiens 81-87 26862579-3 2016 Ang II-induced VSMC ROS production is modulated by alpha1beta1 integrin. ros 20-23 angiotensinogen Homo sapiens 0-6 26862579-4 2016 Ang II also stimulates ROS production in VSMC via p47 (phox) , a NOX2 subunit. ros 23-26 angiotensinogen Homo sapiens 0-6 26862579-7 2016 Ang II effect on ROS production is also PI3K dependent. ros 17-20 angiotensinogen Homo sapiens 0-6 25591955-5 2015 Moreover, treatment of macrophages with 15d-PGJ2, a natural PPAR-gamma ligand, significantly reduced Ang II-induced expression of Egr-1 and its inflammatory gene targets (IL-1beta, TNF-alpha, TGF-beta, MCP-1 and ICAM-1) through PPAR-gamma activation and ROS formation. ros 254-257 angiotensinogen Homo sapiens 101-107 26279425-1 2015 BACKGROUND: Angiotensin II/Angiotensin II type 1 receptor (AT1R) effects are dependent on ROS production stimulated by NADPH oxidase activation. ros 90-93 angiotensinogen Homo sapiens 12-26 25234195-7 2015 Meaningfully, pretreatment of a type of ROS scavenger formulations named N-(mercaptopropionyl)-glycine (N-MPG) could inhibit podocyte apoptosis induced by Ang II. ros 40-43 angiotensinogen Homo sapiens 155-161 24523033-4 2014 In cultured human umbilical vein endothelium cells, Ang II stimulation increased generation of ROS and 4-hydroxy-2-nonenal, both of which were clearly restored by administration of adiponectin. ros 95-98 angiotensinogen Homo sapiens 52-58 27687768-0 2016 Angiotensin-(1-7) abrogates angiotensin II-induced proliferation, migration and inflammation in VSMCs through inactivation of ROS-mediated PI3K/Akt and MAPK/ERK signaling pathways. ros 126-129 angiotensinogen Homo sapiens 28-42 27394920-7 2016 Exposure to 1 muM Ang II for 24 h resulted in mitochondrial depolarization, cytochrome c release, and increased ROS production. ros 112-115 angiotensinogen Homo sapiens 18-24 22693564-10 2012 Importantly, our data point to a critical role for the mitochondria in regulating ROS generation in response to Ang II. ros 82-85 angiotensinogen Homo sapiens 112-118 22217266-8 2012 The antioxidant N-acetyl-L-cysteine reduced ROS production and STAT1 activity induced by Ang II, indicating that Ang II uses ROS as a second messenger to regulate STAT1 activity. ros 44-47 angiotensinogen Homo sapiens 89-95 22217266-8 2012 The antioxidant N-acetyl-L-cysteine reduced ROS production and STAT1 activity induced by Ang II, indicating that Ang II uses ROS as a second messenger to regulate STAT1 activity. ros 44-47 angiotensinogen Homo sapiens 113-119 22217266-8 2012 The antioxidant N-acetyl-L-cysteine reduced ROS production and STAT1 activity induced by Ang II, indicating that Ang II uses ROS as a second messenger to regulate STAT1 activity. ros 125-128 angiotensinogen Homo sapiens 89-95 22217266-8 2012 The antioxidant N-acetyl-L-cysteine reduced ROS production and STAT1 activity induced by Ang II, indicating that Ang II uses ROS as a second messenger to regulate STAT1 activity. ros 125-128 angiotensinogen Homo sapiens 113-119 23516464-7 2013 In conclusion, human PRR over-expression induced ROS production through both angiotensin II-dependent and -independent mechanisms. ros 49-52 angiotensinogen Homo sapiens 77-91 23516464-8 2013 We showed that PRR-mediated angiotensin II-independent ROS formation is associated with activation of the MAPK/ERK1/2 and PI3/Akt signaling pathways and up-regulation of mRNA level of NOX 2 and NOX4 isoforms in neuronal cells. ros 55-58 angiotensinogen Homo sapiens 28-42 23087143-10 2012 Meanwhile, EGCG reduced Ang II- and IL-6-stimulated generation of ROS in macrophages. ros 66-69 angiotensinogen Homo sapiens 24-30 23087143-11 2012 CONCLUSION: EGCG is able to inhibit Ang II- and IL-6-stimulated CRP expression in macrophages to produce an anti-inflammation by interfering with ROS generation. ros 146-149 angiotensinogen Homo sapiens 36-42 20339118-11 2010 Nox5 activation by Ang II and ET-1 induces ROS generation and ERK1/2 phosphorylation. ros 43-46 angiotensinogen Homo sapiens 19-25 20005303-5 2010 In human PMNs, HMR concentration-dependently reduced ROS production induced by either N-formyl-Met-Leu-Phe, phorbol myristate acetate or angiotensin II, as well as interleukin-8 production induced by either N-formyl-Met-Leu-Phe or angiotensin II. ros 53-56 angiotensinogen Homo sapiens 137-151