NAD(P)H oxidase: role in cardiovascular biology and disease.

By K. Griendling, D. Sorescu, M. Ushio-Fukai. Circulation Research, 2000

3,044 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/08856d39c2baff962584db92adfb42f5d1ae7812

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Citations in the corpus

NADPH Oxidases (NOX): An Overview from Discovery, Molecular Mechanisms to Physiology and Pathology (2021, background): “phagocytic NADPH oxidase in a wide variety of cells such as fibroblasts [73], certain tumor cells [74] and vascular tissue cells [75].”
Vitamins C and E: Beneficial effects from a mechanistic perspective (2011, background): “The activity of NADPH oxidase, a major source of superoxide in vascular smooth muscle cells and cardiac myocytes [98], therefore”
Oxidative Stress and Oxidative Damage in Carcinogenesis (2010, background): “…by a variety of endogenous and exogenous stimuli, phagocytes undergo a respiratory burst leading to transient increases in oxygen uptake and generation of ROS through NADPH oxi- dase, the enzyme that catalyzes the single electron reduction of oxygen (Griendling, Sorescu, and Ushio-Fukai 2000).”
Nitric oxide synthases: regulation and function. (2012, background): “135 In addition, the AT 1 receptor is up-regulated in vitro by low-density lipoprotein.”
The effects of oxidative stress on female reproduction: a review (2012, background): “Increased SO anion production through activation of these enzymes may occur through one of several physiological mechanisms, and has been implicated in the pathogenesis of some vascular diseases [209].”
Oxidative stress and reactive oxygen species in endothelial dysfunction associated with cardiovascular and metabolic diseases. (2018, background): “It should be recalled that the major source of ROS in the vascular wall is the membrane-bound NADPH oxidase, which is regulated by vasoactive agents, cytokines, growth factors and mechanical forces [200].”
Reactive oxygen species and angiogenesis: NADPH oxidase as target for cancer therapy. (2008, background): “The neutrophil NADPH oxidase releases large amounts of (O2 ) in bursts, whereas the non-phagocytic NADPH oxidase(s) continuously produce low levels of (O2 ) intracellularly in basal state, yet it can be further stimulated acutely by various agonists and growth factors [31,63].”
Reactive oxygen species in the vasculature: molecular and cellular mechanisms. (2003, background): “If the concentration of L-arginine or H4B is low, or if H4B is oxidized, NOS becomes uncoupled and generates significant amounts of O2· .9 This occurs in hypertension, where activation of NAD(P)H oxidases leads to oxidation of H4B and production of large amounts of O2· from endothelial NOS.10 Xanthi”
Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. (2004, background): “Studies in hypertensive models associated with activation of the renin-angiotensin system have convincingly shown that increased NADPH oxidase activity (at least in part due to increased subunit expression) contributes both to endothelial dysfunction and elevation of blood pressure per se (21, 50, 8”
A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation. (2013, positive): “Proin ﬂ ammatory cytokines are also known to elicit endothelial production of ROS through activation of nicotinamide adenine dinucleotide phosphate oxidases (28).”
Pathogenesis of Diabetic Nephropathy (2004, neutral): “Major enzymatic sources of ROS generation are NADPH oxidases of the nonphagocytic cell types such as endothelial cells, vascular smooth muscle cells, renal mesangial and tubular cells among others [67,68].”