Atherosclerosis and NADPH Oxidase

Nushjira Pongnimitprasert

Department of Pharmacology and Toxicology, Faculty of Pharmacy, Silpakorn University, Nakhon Pathom, Thailand


Vascular diseases including coronary artery disease, cerebrovascular and peripheral vascular diseases are the largest cause of mortality and morbidity. Reactive oxygen species (ROS), especially superoxide (O2•-) have been implicated in the pathogenesis of virtually every stage of vascular lesion formation in atherosclerosis. Atherosclerosis is a disease affecting arterial blood vessels. It is a chronic inflammatory response in the walls of arteries, in large part to the deposition of lipoproteins (plasma proteins that carry cholesterol and triglycerides). Oxidation of low density lipoprotein (LDL) was injurious to artery wall cells and suggested that LDL oxidation might be important in atherogenesis. Among the potential sources of ROS, the NADPH oxidases appear to be especially important for redox signalling and indeed possess several biochemical properties that make them well suited for involvement in signal transduction. The NADPH oxidase system plays a key role in generating ROS, including O2•- and hydrogen peroxide (H2O2) in phagocytic cells, fibroblasts, vascular smooth muscle cells, and endothelial cells. The NADPH oxidase system is regulated systemically in veins and arteries, which strengthens the importance of the molecular regulation of the enzyme in cardiovascular disease (CVD), especially atherosclerosis.

Key Words: Atherosclerosis; NADPH oxidase; ROS

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