Angiotensin II Stimulation of NAD(P)H Oxidase Activity: Upstream Mediators

By P. Seshiah, D. Weber, Petra Ročić, Liisa Valppu, Y. Taniyama, K. Griendling. Circulation Research, 2002

770 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Endocrinology, Diabetes and Metabolism, Physiology

View Paper: https://www.semanticscholar.org/paper/d205b64de03531784f86c782ff1c38d0fe43b8f3

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In Cardiology and Cardiovascular Medicine

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Citations in the corpus

Reactive Oxygen Species in Inflammation and Tissue Injury (2014, positive): “Rac1 activation is induced by a variety of inflammatory stimuli such as TNF-a (453), interleukin-1b (IL-1b), thrombin, VEGF (299), histamine (321), Ang II (384), ischemia-reperfusion injury (216), and shear stress (463).”
Vascular NAD(P)H oxidases: specific features, expression, and regulation. (2003, background): “Although the vascular enzyme is activated within minutes of stimulation (107, 168, 231), its activity can also be markedly upregulated in the hours after exposure to agonists.”
Reactive oxygen species in vascular biology: implications in hypertension (2004, positive): “2002a), the adventitia (Rey and Pagano 2002), and in cultured VSMCs, fibroblasts, and endothelial cells (Griendling et al. 1994; Seshiah et al. 2002; Touyz et al. 2002a).”
Oxygen, oxidative stress, hypoxia, and heart failure. (2005, background): “and TNF-α, for example, can induce H2O2 and O2•– formation via activation of the NAD(P)H oxidases (10, 15).”
ADAMs as mediators of EGF receptor transactivation by G protein-coupled receptors. (2006, background): “In addition, Src, cAbl, and phosphorylation of the AT1 at Tyr(319) are required for ANG II-induced EGFR transactivation (88, 89, 106).”
Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system. (2007, background): “ANG II-mediated activation of NAD(P)H oxidases involves the upstream mediators Src/EGFR/PI3K/ Rac-1 (discussed below) and PLD/PKC/p47phox phosphorylation (174, 195).”
NADPH Oxidases in Cardiovascular Health and Disease (2006, neutral): “In the case of Nox-based oxidase activity in EC, isolated increases in Nox2 may be sufficient since Nox2 mRNA expression level is low compared to other oxidase subunits (290).”
Nox proteins in signal transduction (2009, positive): “Nox5 signal transduction pathways Nox5 is activated by PKC, IP3 and Ca2+ produced by PDGFR activation and cytokine receptor activation (IL-4/IL-4R).”
Redox signaling in hypertension. (2006, background): “[29] Seshiah PN, Weber DS, Rocic P, Valppu L, Taniyama Y, Griendling KK.”
Crosstalk between mitochondria and NADPH oxidases (2011, background): “Indeed, activation of NADPH oxidases has been reported to be a biphasic process inwhich the first phase requires direct activation by AngII followed by a second phase of sustained activation that is H2O2 dependent [104].”