Circulation. 2003;108:1912-1916
doi: 10.1161/01.CIR.0000093660.86242.BB
doi: 10.1161/01.CIR.0000093660.86242.BB
(Circulation. 2003;108:1912.)
© 2003 American Heart Association, Inc.
Review: Clinical Cardiology: New Frontiers |
Oxidative Stress and Cardiovascular Injury
Part I: Basic Mechanisms and In Vivo Monitoring of ROS
From the Division of Cardiology (K.K.G.), Emory University, Atlanta, Ga, and the Center for Experimental Therapeutics (G.A.F.), University of Pennsylvania, Philadelphia, Pa.
Correspondence to Garret A. FitzGerald, MD, Center for Experimental Therapeutics, 153 Johnson Pavilion, University of Pennsylvania, 3620 Hamilton Walk, Philadelphia, PA 19104-6084. E-mail garret@spirit.gcrc.upenn.edu
Key Words: oxygen • reactive oxygen species • atherosclerosis • hypertension • restenosis
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Oxidative stress has been associated with diverse pathophysiological events, including cancer, renal disease, and neurodegeneration. More recently, it has become apparent that reactive oxygen species (ROS) also play a role in the development of vasculopathies, including those that define atherosclerosis, hypertension, and restenosis after angioplasty. The "response to injury" hypothesis developed by Russell Ross in the late 1970s suggested that atherosclerosis, at least, resulted from an initial injury to endothelial cells, leading to impaired endothelial function and subsequent macrophage infiltration and smooth muscle dysfunction. Many investigators then focused on oxidation of LDL and its interaction with the endothelium as the initial injury leading to the formation of fatty streaks and ultimately atherogenesis. It is now clear not only that diverse ROS are produced in the vessel wall, but that they individually and in combination contribute to many of the abnormalities associated with vascular disease.
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Reactive Oxygen Species |
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There are many ROS that play central roles in vascular physiology (Figure 1) and pathophysiology, the most important of which are nitric oxide (NO·), superoxide (O2·-), hydrogen peroxide (H2O2) and peroxynitrite (ONOO·-). NO· is normally produced by endothelial nitric oxide synthase (eNOS) in the vasculature, but in inflammatory states, inducible NOS can be expressed in macrophages and smooth muscle cells and contributes to NO·production. NO·is a crucial mediator of endothelium-dependent vasodilation and may also play a role in platelet aggregation and in maintaining the balance between smooth muscle cell growth and differentiation. Superoxide results from one electron reduction of oxygen
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