Journal
CIRCULATION RESEARCH
Volume 96, Issue 8, Pages 818-822Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.RES.0000163631.07205.fb
Keywords
reactive oxygen species; hydrogen peroxide (H2O2); endothelial function; vascular NAD(P)H oxidases; Nox; uncoupled endothelial nitric oxide synthase (eNOS) atherosclerosis
Funding
- NHLBI NIH HHS [R01 HL077440] Funding Source: Medline
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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 (O-2(center dot-)) and hydrogen peroxide ( H2O2) appear most important in redox signaling. Whereas O-2(center dot-) predominantly induces endothelial dysfunction by rapidly inactivating nitric oxide (NO center dot), H2O2 influences different aspects of endothelial cell function via complex mechanisms. This review discusses recent advances establishing a critical role of H2O2 in the development of vascular disease, in particular, atherosclerosis, and mechanisms whereby vascular NAD(P) H oxidase-derived H2O2 amplifies its own production. Recent studies have shown that H2O2 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 H2O2-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 for NAD( P) H oxidases, representing a family of novel NAD( P) H oxidases].
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