Cardiovascular Research

Cardiovascular Research 2005 68(1):26-36; doi:10.1016/j.cardiores.2005.06.021

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Copyright © 2005, European Society of Cardiology

Hydrogen peroxide regulation of endothelial function: Origins, mechanisms, and consequences

Hua Cai^*

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

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Time for primary review 27 days

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