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 &À ) in vascular cells. While some O 2 &À rapidly degrades by reacting with nitric oxide (NO & ), the O 2 &À signal preserved by dismutation into hydrogen peroxide (H 2 O 2 ) exerts

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... longed signaling effects. This review focuses on patterns and mechanisms whereby H 2 O 2 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 H 2 O 2 contribution to the development of vascular disease.