This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Channon, K. M. Search for Related Content PubMed PubMed Citation Articles by Channon, K. M.

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1751.)
© 2002 American Heart Association, Inc.

Editorials

Oxidative Stress and Coronary Plaque Stability

Keith M. Channon

From the Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK.

Correspondence to Professor K.M. Channon, Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK. E-mail keith.channon@cardiov.ox.ac.uk

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

Increased production of reactive oxygen species (ROS) in the vascular wall is a characteristic feature of disease states, including atherosclerosis, diabetes and hypertension. ROS, such as superoxide, reduce nitric oxide bioactivity by scavenging and cause oxidation of lipids and target proteins. In addition, recent work has revealed that ROS mediate a wide range of pathological processes in the endothelium, smooth muscle cells, and inflammatory cells.¹ ROS are generated by enzyme systems present in cells in the vascular wall, including NAD(P)H oxidase, xanthine oxidase, and nitric oxide synthase. The activities and levels of these enzyme systems are increased in association with vascular disease risk factors² and in vascular disease states in which oxidative stress is prominent, for example, in diabetes³ and atherosclerosis.

See page 1838

The NAD(P)H oxidases appear to be particularly important sources of ROS production in blood vessels,⁴ where they are constitutively active, producing relatively low levels of ROS under basal conditions, but generating higher levels of oxidants in response to stimuli such as growth factors and cytokines. These factors are consistent with a role for nonphagocytic NAD(P)H oxidases in cellular signaling rather than the high-level burst activity characteristic of the phagocyte NAD(P)H oxidase. The NAD(P)H oxidases are multimeric enzymes composed of plasma membrane associated–proteins as well as cytosolic factors. In the phagocytic-type NAD(P)H oxidase, the plasma membrane–associated proteins gp91phox and p22phox compose the flavocytochrome b558 complex, which forms the catalytic subunit of the oxidase. The cytosolic subunits, including p47phox, p67phox, and the G-protein Rac, provide regulatory function.

Azumi . . . [Full Text of this Article]

This article has been cited by other articles:

				K. Bedard and K.-H. Krause The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology Physiol Rev, January 1, 2007; 87(1): 245 - 313. [Abstract] [Full Text] [PDF]

				N. R. Madamanchi, A. Vendrov, and M. S. Runge Oxidative Stress and Vascular Disease Arterioscler Thromb Vasc Biol, January 1, 2005; 25(1): 29 - 38. [Abstract] [Full Text] [PDF]

				K. Suzuki, Y. Ito, K. Wakai, M. Kawado, S. Hashimoto, H. Toyoshima, M. Kojima, S. Tokudome, N. Hayakawa, Y. Watanabe, et al. Serum Oxidized Low-Density Lipoprotein Levels and Risk of Colorectal Cancer: A Case-Control Study Nested in the Japan Collaborative Cohort Study Cancer Epidemiol. Biomarkers Prev., November 1, 2004; 13(11): 1781 - 1787. [Abstract] [Full Text] [PDF]

				P. Stenvinkel, R. Pecoits-Filho, and B. Lindholm Coronary Artery Disease in End-Stage Renal Disease: No Longer a Simple Plumbing Problem J. Am. Soc. Nephrol., July 1, 2003; 14(7): 1927 - 1939. [Full Text] [PDF]

				Z S Nedeljkovic, N Gokce, and J Loscalzo Mechanisms of oxidative stress and vascular dysfunction Postgrad. Med. J., April 1, 2003; 79(930): 195 - 200. [Abstract] [Full Text] [PDF]