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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.R800087-JLR200 on November 15, 2008

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Journal of Lipid Research, Vol. 50, S376-S381, April 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Atherogenesis

The LDL modification hypothesis of atherogenesis: an update

Daniel Steinberg1

Department of Medicine, University of California San Diego, La Jolla, CA

Published, JLR Papers in Press, November 15, 2009.

1 To whom correspondence should be addressed. e-mail: dsteinberg{at}ucsd.edu


ABSTRACT

The accumulated evidence that oxidative modification of LDL plays an important role in the pathogenesis of atherosclerosis in animal models is very strong. The negative results in recent clinical studies have caused many to conclude that LDL oxidation may not be relevant in the human disease. Yet many of the lines of evidence that support the hypothesis have been demonstrated to apply also in humans. In this review, we briefly summarize the lines of evidence on which the hypothesis rests, its strengths, and its weaknesses.

Supplementary key words atherosclerosis • pathogenesis • macrophages • foam cells • fatty streak • clinical trials • antioxidants • 12/15-lipoxygenase • 5-lipoxygenase • animal models

Abbreviations: apo, apolipoprotein; M-CSF, macrophage-colony-stimulating factor; SRA, scavenger receptor A


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JLR 50th Anniversary Collections
Anniversary Collection::Atherogenesis

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