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(Circulation Research. 2003;93:183.)
© 2003 American Heart Association, Inc.

Editorials

United They Go

Conjunct Regulation of Aortic Antioxidant Enzymes During Atherogenesis

Wulf Palinski

From the Department of Medicine, University of California San Diego, La Jolla, Calif.

Correspondence to Wulf Palinski, MD, Department of Medicine, 0682, University of California San Diego, 9500 Gilman Dr MTF 110, La Jolla, CA 92093-0682. E-mail wpalinski@ucsd.edu

Key Words: atherosclerosis • pathophysiology • oxidation • gene expression

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

Oxidative stress, resulting from a local imbalance between the ubiquitous formation of reactive oxygen species (ROS) and the equally ubiquitous antioxidant defenses, is thought to be an important contributor to atherogenesis (Figure). Many of the players are known. The biochemical pathways generating superoxide, hydrogen peroxide, hydroxyl radicals, and lipid peroxides have been identified, as have the most important oxygen radical–scavenging enzymes (superoxide dismutase, catalase, glutathione peroxidase, and thioredoxin reductase).¹ Many endogenous and exogenous contributors to oxidative stress are also known, such as hypercholesterolemia, hyperglycemia, hypertension, and shear stress. Leukocytes responding to intimal signals—frequently resulting from increased oxidation—are also an important contributor to ROS formation. In fact, ROS released during the respiratory burst, an innate immune defense against bacterial pathogens, may promote lipid peroxidation and therefore enhance further leukocyte recruitment and differentiation. In addition to antioxidant enzymes, arterial cells express enzymes promoting ROS formation, including, cyclooxygenase, NADPH oxidase, cytochrome P450 epoxygenases, myeloperoxidase, lipoxygenase, and inducible nitric oxide synthase.^1–3 To what extent these enzymes account for ROS formation and oxidation of LDL in arteries, however, remains unknown. Dietary factors, natural and synthetic antioxidants, and hypocholesterolemic agents, such as statins, also directly and indirectly influence ROS.

View larger version (36K): [in this window] [in a new window]   Reactive oxygen species (ROS) in the arterial wall. Intrinsic and extrinsic factors influencing ROS formation and mechanisms through which ROS may affect atherogenesis.

Research in vitro and in vivo has also shed much light on potential mechanisms through which oxidative stress may promote atherogenesis. Initially, the oxidation of LDL was seen as the central event.³ . . . [Full Text of this Article]

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