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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.R800036-JLR200 on October 27, 2008

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Journal of Lipid Research, Vol. 50, S145-S149, April 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology


Lipoprotein Metabolism

The role of dysfunctional HDL in atherosclerosis

Mohamad Navab1,*, Srinivasa T. Reddy*, Brian J. Van Lenten*, G. M. Anantharamaiah{dagger} and Alan M. Fogelman*

* Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679
{dagger} Atherosclerosis Research Unit, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294

This work was supported in part by US Public Health Service grants HL-30568 and HL-34343 and the Laubisch, Castera, and M.K. Grey Funds at UCLA. M.N., S.T.R., G.M.A. and A.M.F. are principals in Bruin Pharma and A.M.F. is an officer in Bruin Pharma.

Published, JLR Papers in Press, October 27, 2008.

1 To whom correspondence should be addressed. e-mail: mnavab{at}mednet.ucla.edu


ABSTRACT

This review focuses on HDL function in modulating LDL oxidation and LDL-induced inflammation. Dysfunctional HDL has been identified in animal models and humans with chronic inflammatory diseases including atherosclerosis. The loss of antiinflammatory function correlated with a loss of function in reverse cholesterol transport. In animal models and perhaps in humans, dysfunctional HDL can be improved by apoA-I mimetic peptides that bind oxidized lipids with high affinity.

Supplementary key words inflammation • high density lipoprotein • LDL • mimetic peptides • L-4F • D-4F

Abbreviations: apo, apolipoprotein; CHD, coronary heart disease; HII, HDL-inflammatory index; HPETE, hydroperoxyeicosatetraenoic acid; HPODE, hydroperoxyoctadecadienoic acid; 12-LO, 12-lipoxygenase; MCP-1, monocyte chemoattractant-1; PAPC, 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine; PON, paraoxonase


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JLR 50th Anniversary Collections
Anniversary Collection::Lipoprotein Metabolism

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