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Journal of Lipid Research, Vol. 50, S145-S149, April 2009
The role of dysfunctional HDL in atherosclerosis
* Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679 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
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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