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Originally published In Press as doi:10.1194/jlr.R800086-JLR200 on December 16, 2008

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Journal of Lipid Research, Vol. 50, S346-S351, April 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Atherogenesis

Myeloperoxidase, modified lipoproteins, and atherogenesis

Stephen J. Nicholls and Stanley L. Hazen1

Departments of Cell Biology and Cardiovascular Medicine, Center for Cardiovascular Diagnostics and Prevention, Cleveland Clinic, Cleveland, OH

Published, JLR Papers in Press, December 16, 2008.

1 To whom correspondence should be addressed. e-mail: hazens{at}ccf.org


ABSTRACT

Numerous lines of evidence implicate a role for myeloperoxidase (MPO) in the pathogenesis of atherosclerosis. Enriched within vulnerable plaque, MPO serves as an enzymatic source of eicosanoids and bioactive lipids and generates atherogenic forms of both low- and high-density lipoproteins. These factors likely contribute to clinical studies demonstrating that increased systemic levels of MPO and its oxidation products predict increased cardiovascular risk. As a result, interest has focused on the potential to target MPO for the development of new risk markers, imaging, and therapies to prevent cardiovascular events.

Supplementary key words oxidant stress • free radicals • scavenger receptor • high density lipoprotein

Abbreviations: apoA-I, apolipoprotein A-I; CVD, cardiovascular disease; MPO, myeloperoxidase


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JLR 50th Anniversary Collections
Anniversary Collection::Atherogenesis

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