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Excessive production of reactive oxygen species in the vasculature contributes to cardiovascular pathogenesis. Among biologically relevant and abundant reactive oxygen species, superoxide (O2 ·− ) and hydrogen peroxide (H2 O2 ) appear most important in redox signaling. Whereas O2 ·− predominantly induces endothelial dysfunction by rapidly inactivating nitric oxide (NO· ), H2 O2 influences different aspects of endothelial cell function via complex mechanisms. This review discusses recent advances establishing a critical role of H2 O2 in the development of vascular disease, in particular, atherosclerosis, and mechanisms whereby vascular NAD(P)H oxidase–derived H2 O2 amplifies its own production. Recent studies have shown that H2 O2 stimulates reactive oxygen species production via enhanced intracellular iron uptake, mitochondrial damage, and sources of vascular NAD(P)H oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase (eNOS). This self-propagating phenomenon likely prolongs H2 O2 -dependent pathological signaling in vascular cells, thus contributing to vascular disease development. The latest progress on Nox functions in vascular cells is also discussed [Nox forN AD(P)Hox idases, representing a family of novel NAD(P)H oxidases].

NAD(P)H Oxidase–Dependent Self-Propagation of Hydrogen Peroxide and Vascular Disease