Published online before print October 2, 2003, doi: 10.1161/01.ATV.0000097769.47306.12
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© 2004 American Heart Association, Inc.
Brief Reviews |
Regulation of Superoxide Anion Production by NADPH Oxidase in Monocytes/Macrophages
Contributions to Atherosclerosis
From the Department of Cell Biology, Cleveland Clinic Foundation, Cleveland, Ohio.
Correspondence to Martha K. Cathcart, PhD, Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195. E-mail cathcam{at}ccf.org
Series Editor: Marschall S. Runge
ATVB In Focus
Extracellular Mediators in Atherosclerosis and Thombosis
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Monocyte extravasation into the vessel wall has been shown to be a critical step in the development of atherosclerosis. Upon activation, monocytes produce a burst of superoxide anion due to activation of the NADPH oxidase enzyme complex. Monocyte-derived superoxide anion contributes to oxidant stress in inflammatory sites, is required for monocyte-mediated LDL oxidation, and alters basic cell functions such as adhesion and proliferation. We hypothesize that monocyte-derived superoxide anion production contributes to atherosclerotic lesion formation. In this brief review, we summarize our current understanding of the signal transduction pathways regulating NADPH oxidase activation and related superoxide anion production in activated human monocytes. Novel pathways are identified that may serve as future targets for therapeutic intervention in this pathogenic process. The contributions of superoxide anion and NADPH oxidase to atherogenesis are discussed. Future experiments are needed to clarify the exact role of NADPH oxidase-derived superoxide anion in atherogenesis, particularly that derived from monocytes.
Key Words: monocyte • macrophage • superoxide anion • NADPH oxidase • atherosclerosis
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