The regulation of endothelial function plays an important role in the development
and progression of metabolic and cardiovascular diseases. A critical determinant of
endothelial function is the balance between nitric oxide and reactive oxygen species.
Endothelium-derived NO availability can be limited by enhanced formation of reactive
oxygen species. Major sources of reactive oxygen species in the vessel wall are NAD(P)H
oxidase complexes. This review summarizes the impact of vascular NAD(P)H oxidase-derived
reactive oxygen species on atherosclerosis and endothelial dysfunction. Changes in
NAD(P)H oxidase expression and activity have clinical implications. Mutations in NAD(P)H
oxidase subunits can lead to impaired oxidative burst in leukocytes and chronic granulomatous
disease. In contrast, normalization of increased expression and activity of NAD(P)H
oxidase in endothelial dysfunction and vascular disorders can be considered as a novel
therapeutic strategy in the treatment of cardiovascular diseases.
endothelial dysfunction - cardiovascular system - vessel wall - nitric oxide - oxidative
stress - reactive oxygen species - NAD(P)H oxidase