How Vascular NAD(P)H Oxidase Activity and Nox Isoform Expression are Regulated
This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
It is well known that endothelial dysfunction is a systemic disorder and a key variable in the initiation and progression of atherosclerosis and its complications.1 Most risk factors that are related to atherosclerosis and cardiovascular morbidity and mortality, including hypercholesterolemia, hypertension, cigarette smoking, and diabetes mellitus, are found to be associated with endothelial dysfunction. Some studies have shown that the risk for developing endothelial dysfunction increases with the number of risk factors present in an individual. Endothelial dysfunction is not confined to the coronary arteries but rather represents a systemic disorder that also affects peripheral vascular beds, including both conduit arteries and small resistance vessels in the extremities. Therefore, a uniform underlying mechanism(s) is suggested to account for the impaired endothelial function.
See page 1614
Recent studies have demonstrated that increased production of reactive oxygen species in human blood vessels is associated with endothelial dysfunction. The major source of superoxide anion in the vasculature is NAD(P)H oxidase family of enzymes. NAD(P)H oxidases are present in the vascular cells including endothelial cells, smooth muscle cells, fibroblasts, and macrophages.2 Vascular NAD(P)H oxidase is a multisubunit enzyme complex that differs structurally and biochemically from the phagocytic NAD(P)H oxidase. This superoxide-generating enzyme includes the membrane-bound flavocytochrome b558 …