Hydrogen peroxide regulation of endothelial function: origins, mechanisms, and consequences.
作者： H CAI
DOI: 10.1016/J.CARDIORES.2005.06.021
关键词:
摘要: Increased production of reactive oxygen species (ROS) has been implicated in the pathogenesis cardiovascular diseases. Enzymatic systems such as mitochondrial respiratory chain, vascular NAD(P)H oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase (eNOS) produce superoxide anion (O2.−) cells. While some O2.− rapidly degrades by reacting with (NO.), signal preserved dismutation into hydrogen peroxide (H2O2) exerts prolonged signaling effects. This review focuses on patterns mechanisms whereby H2O2 modulates different aspects cell function including growth proliferation, apoptosis, endothelium-dependent vasorelaxation, cytoskeletal reorganization barrier dysfunction, inflammatory responses, endothelium-regulated remodeling. These modulations may at least partially underlie contribution to development disease.
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