Copyright © 2005, European Society of Cardiology
Hydrogen peroxide regulation of endothelial function: Origins, mechanisms, and consequences
Section of Cardiology, Department of Medicine, The Division of Biological Sciences and Pritzker School of Medicine, The University of Chicago, 5841 S Maryland Ave, MC6088, Chicago, IL, 60637, United States
* Tel.: +1 773 834 0705; fax: +1 773 702 2681. Email address: lcai{at}medicine.bsd.uchicago.edu hcai{at}medicine.bsd.uchicago.edu
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 (O2.–) in vascular cells. While some O2.– rapidly degrades by reacting with nitric oxide (NO.), the O2.– 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.
KEYWORDS 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
Time for primary review 27 days
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