期刊
CARDIOVASCULAR RESEARCH
卷 68, 期 1, 页码 26-36出版社
OXFORD UNIV PRESS
DOI: 10.1016/j.cardiores.2005.06.021
关键词
hydrogen peroxide; endothelial function; superoxide; nitric oxide; growth; actin cytoskeleton; barrier function; inflammation; vascular remodeling; vascular NAD(P)H oxidases; uncoupled endothelial nitric oxide synthase; xanthine oxidase; mitochondrion; Nox
资金
- NHLBI NIH HHS [R01 HL077440] Funding Source: Medline
Increased production of reactive oxygen species (ROS) has been implicated in the pathogenesis of cardiovascular diseases. Enzymatic systems such as the mitochondrial respiratory chain, vascular NAD(P)H oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase (eNOS) produce superoxide anion (O-2(-)) in vascular cells. While some O-2(-) rapidly degrades by reacting with nitric oxide (NO), the O-2(-) signal preserved by dismutation into hydrogen peroxide (H2O2) exerts prolonged signaling effects. This review focuses on patterns and mechanisms whereby H2O2 modulates different aspects of endothelial cell function including endothelial cell growth and proliferation, endothelial apoptosis, endothelium-dependent vasorelaxation, endothelial cytoskeletal reorganization and barrier dysfunction, endothelial inflammatory responses, and endothelium-regulated vascular remodeling. These modulations of endothelial cell function may at least partially underlie H2O2 contribution to the development of vascular disease. (c) 2005 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
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