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Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1102-1111
Published online before print March 24, 2005, doi: 10.1161/01.ATV.0000163262.83456.6d
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Right arrow Redox Mechanisms in Blood Vessels
(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1102.)
© 2005 American Heart Association, Inc.


Brief Reviews

Myeloperoxidase and Cardiovascular Disease

Stephen J. Nicholls; Stanley L. Hazen

From the Departments of Cardiovascular Medicine and Cell Biology and Center for Cardiovascular Diagnostics and Prevention, Cleveland Clinic Foundation, Cleveland, Ohio.

Correspondence to Stanley L. Hazen, MD, PhD, Cleveland Clinic Foundation, Lerner Research Institute, Center for Cardiovascular Diagnostics and Prevention, 9500 Euclid Avenue, NC-10, Cleveland, OH 44195. E-mail hazens{at}ccf.org

Series Editor: Kathy K. Griendling
Redox Mechanisms in Blood Vessels
ATVB in Focus

Previous Brief Reviews in this Series:

•Mueller CFH, Laude K, McNally JS, Harrison DG. Redox mechanisms in blood vessels. 2005;25:274–278.
•Gutterman DD, Miura H, Liu Y. Redox modulation of vascular tone: focus of potassium channel mechanisms of dilation. 2005;25:671–678.

Myeloperoxidase (MPO) is a leukocyte-derived enzyme that catalyzes the formation of a number of reactive oxidant species. In addition to being an integral component of the innate immune response, evidence has emerged that MPO-derived oxidants contribute to tissue damage during inflammation. MPO-catalyzed reactions have been attributed to potentially proatherogenic biological activities throughout the evolution of cardiovascular disease, including during initiation, propagation, and acute complication phases of the atherosclerotic process. As a result, MPO and its downstream inflammatory pathways represent attractive targets for both prognostication and therapeutic intervention in the prophylaxis of atherosclerotic cardiovascular disease.

Myeloperoxidase-catalyzed reactions have been attributed to potentially proatherogenic biological activities throughout the evolution of cardiovascular disease, including during initiation, propagation, and acute complication phases of the atherosclerotic process. As a result, myeloperoxidase and its downstream inflammatory pathways represent attractive targets for both prognostication and therapeutic intervention in the prophylaxis of atherosclerotic cardiovascular disease.


Key Words: atherosclerosis • free radical • heart failure • high-density lipoprotein • low-density lipoprotein • myeloperoxidase • nitric oxide • scavenger receptor • vulnerable plaque




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