Vascular superoxide production by NAD(P)H oxidase: association with endothelial dysfunction and clinical risk factors.

By T. Guzik, Nicky West, E. Black, D. McDonald, C. Ratnatunga, R. Pillai, K. Channon. Circulation Research, 2000

648 citations recorded by the source corpus.

Subfields: Biophysics, Physiology

View Paper: https://www.semanticscholar.org/paper/126d69ccb0ac8d30b493409c63c66f638534dcf1

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Physiology

1. R. Clempus
2. A. Shah
3. B. Lassègue
4. C. van Dijk
5. T. Berl
6. Jian-Mei Li
7. T. Guzik
8. Rhian M. Touyz

Citations in the corpus

• NADPH Oxidases in Cardiovascular Health and Disease (2006, positive): “Several recent studies have provided confirmatory evidence of important pathophysiological roles for NADPH oxidases in human cardiovascular disease (128, 137, 224, 316).”
• Nitric oxide and superoxide in inflammation and immune regulation. (2003, background): “In the absence of BH4, NOS produce superoxide, instead of nitric oxide (5, 6).”
• Vascular NAD(P)H oxidases: specific features, expression, and regulation. (2003, background): “It is also possible that oxidase activity might be limited in vascular cells by the cytosolic concentrations of NADH and NADPH, as suggested by the increase in superoxide production observed when these substrates were added to whole cells or tissues (13, 58, 68, 69, 76, 113, 146, 148, 182, 183, 224)”
• Pathogenesis of Diabetic Nephropathy (2004, positive): “Diabetes and hyperlipidemia were independently associated with NADPH oxidase-derived ROS generation in this study [69].”
• The role of oxidative stress in atherosclerosis. (2009, background): “It consists of five subunits: p40PHOX (PHOX= phagocyte oxidase), p47PHOX, p67PHOX, p22PHOX and Nox.14 It is reg- ulated by a variety of pathophysiological stimulations relevant to atherosclerosis, such as angiotensin II, thrombin, platelet-derived growth factor, tumor necrosis factor-alpha, and natu”
• Increased myocardial NADPH oxidase activity in human heart failure. (2003, background): “Reactive oxygen species production by the NADPH oxidase in smooth muscle and endothelial cells of the vessel wall has been implicated in the genesis of hypertensive vascular smooth muscle hypertrophy (13,15,16), atherosclerosis (17), and endothelial dysfunction (18).”
• Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. (2004, background): “Endothelial NADPH oxidase activity is increased by 1) mechanical forces such as oscillatory shear stress (67); 2) hypoxia-reoxygenation (77, 136, 141), flow cessation (111), membrane depolarization (4, 140), nutrient deprivation (106), or ischemia (4, 111); 3) G protein-coupled receptor agonists suc”