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Editorial Inflammation and Vascular Hypertrophy Induced by Angiotensin II Role of NADPH Oxidase-Derived Reactive Oxygen Species Independently of Blood Pressure Elevation? Ernesto L. Schiffrin, Rhian M. Touyz vidence from the last few years has suggested that macrophage NAD(P)H oxidase is composed of five subunits: increased oxidative stress plays a pathophysiological p40phox (phox for PHagocyte OXidase), p47phox, p67phox, E role in cardiovascular disease, including atherosclero- p22phox, and gp91phox (Figure). p40phox, p47phox, and 1,2 sis, hypertension, and heart failure. At the same time, p67phox exist in the cytosol, whereas p22phox and gp91phox emerging data have implicated inflammation as a process are located in the cell membrane as an heterodimeric fla- involved in the initiation and progression of atherosclerosis, voprotein, cytochrome b558. When cells are stimulated, but it is also present in hypertension, diabetes mellitus, and p47phox is phosphorylated, and the cytoplasmic complex other conditions associated with vascular damage. A large translocates to the membrane and associates with cytochrome body of data has suggested that the renin-angiotensin system b558 to generate the active oxidase. Activation requires the mediates part of its physiological and pathophysiological participation of two low–molecular weight guanine nucleo- actions via generation of reactive oxygen species (ROS) and tide-binding proteins,
Arteriosclerosis, Thrombosis, and Vascular Biology – Wolters Kluwer Health
Published: May 1, 2003
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