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(Circulation. 2005;112:2585-2588.)
© 2005 American Heart Association, Inc.

Editorial

Oxidative Stress and the Vascular Wall

NADPH Oxidases Take Center Stage

John F. Keaney, Jr, MD

From the Evans Memorial Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Mass.

Correspondence to John F. Keaney, Jr, MD, Evans Memorial Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, 02118. E-mail jkeaney@bu.edu

Key Words: Editorials • calcium • NADPH oxidase • stress

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The contemporary notion that oxidative stress contributes to vascular wall pathology dates back some 25 years, when chemical modification of LDL was found to permit macrophage foam cell formation,¹ and subsequent data indicated that vascular cells promoted LDL lipid oxidation (eg, LDL oxidation) to produce a similarly modified LDL.² It is now clear, however, that oxidative stress in the vascular wall involves much more than the oxidation of LDL lipids. Risk factors for atherosclerosis are associated with an increased arterial wall flux of reactive oxygen species that not only may oxidize biological targets (ie, lipids), but also directly produce phenotypic changes in vascular cells such as inducing smooth muscle cell proliferation, adhesion molecule expression, and premature senescence.³ Many of these cellular responses have been implicated in both the development and the clinical manifestations of atherosclerosis.

Articles pp 2668 and 2677

In the cellular environment, the most common reactive oxygen species produced is superoxide (O₂·^–) because it is the product of a single electron added to oxygen. Cells and tissues contain abundant superoxide dismutase that converts superoxide to hydrogen peroxide (H₂O₂), a species that has garnered considerable interest as an endogenous signaling molecule. A landmark study by Sundaresan and colleagues⁷ demonstrated a requirement for intracellular H₂O₂ generation in the mitogenic effects of platelet-derived growth factor on smooth muscle. Subsequent investigation points to a host of phenotypic responses that involve intracellular reactive oxygen species as signaling molecules (reviewed by Chen et al⁸). As a result of . . . [Full Text of this Article]

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