A gp91phox containing NADPH oxidase selectively expressed in endothelial cells is a major source of oxygen radical generation in the arterial wall.

By A. Görlach, R. Brandes, Kytai Truong Nguyen, M. Amidi, F. Dehghani, R. Busse. Circulation Research, 2000

637 citations recorded by the source corpus.

Subfields: Immunology, Pathology and Forensic Medicine, Physiology

View Paper: https://www.semanticscholar.org/paper/fbdafd067e37164598c9170d6c5dd6f4a69fb3c1

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Citations in the corpus

Activation of NADPH oxidase by AGE links oxidant stress to altered gene expression via RAGE. (2001, neutral): “gp91phox-containing NADPH oxidase (8) support our”
Anti-Inflammatory Effects of Statins: Clinical Evidence and Basic Mechanisms (2005, background): “By inhibiting Rac isoprenylation, statins can lead to a reduction in NADPH oxidase assembly and, consequently, generation of RO”
Vascular oxidative stress, nitric oxide and atherosclerosis. (2014, background): “However, neither the native nor the angiotensin II-driven atherosclerosis is affected by endothelial Nox2 overexpression [43].”
Modulation of Protein Kinase Activity and Gene Expression by Reactive Oxygen Species and Their Role in Vascular Physiology and Pathophysiology (2000, neutral): “p22phox 1 (13, 115) 1 (13) 1 (13, 112, 113) 1 (13) ND 1 (114)”
Crosstalk between mitochondria and NADPH oxidases (2011, background): “Nox2, previously known as gp91phox, is present in endothelial and phagocytic cells [88–91].”
NADPH Oxidases in Cardiovascular Health and Disease (2006, neutral): “Nox5 was reported to be present in EC and cardiac fibroblasts in some studies (8, 20, 57, 111, 348) but there are no reports to date of either Nox3 or Duox2 expression in cardiovascular cells.”
The Role of Oxidative Stress in Neurodegenerative Diseases (2015, background): “For instance, Nox4 and Nox2 are abundant, whereas Nox1 is less in endothelial cells [23, 24].”
Vascular NAD(P)H oxidases: specific features, expression, and regulation. (2003, methodology): “However, gp91phox was not upregulated during the early stage of the disease (188) as might be expected, since the early development of vascular lesions is characterized by proliferation of cells related to VSMC, which do not express gp91phox in either culture or arterial media (32, 58, 81, 90, 107, ”
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”