Format

Send to

Choose Destination
Curr Opin Lipidol. 2002 Aug;13(4):363-72.

Oxidized lipids as mediators of coronary heart disease.

Author information

1
Department of Medicine, Cardiology, University of California Los Angeles, 90095-1679, USA. mnavab@mednet.ucla.edu

Erratum in

  • Curr Opin Lipidol. 2002 Oct;13(5):589. Ready Srinu T [corrected to Reddy Srinu T].

Abstract

PURPOSE OF REVIEW:

To summarize the recent evidence on the physiological relevance of the view that LDL lipid oxidation may play a major role in the inflammatory reaction that leads to or amplifies atherogenesis. Oxidation of LDL phospholipids containing arachidonic acid at the sn-2 position occurs when a critical concentration of 'seeding molecules' derived from the lipoxygenase pathway is reached in LDL. This generates a series of biologically active, oxidized phospholipids that mediate the cellular events seen in the developing fatty streak.

RECENT FINDINGS:

We have observed that LDL from mice that are genetically predisposed to diet-induced atherosclerosis is highly proinflammatory when the mice are maintained on an atherogenic diet, when they are injected with LDL-derived oxidized phospholipids, or once they are infected with influenza A virus. Patients with coronary atherosclerosis also had highly proinflammatory LDL, despite having normal blood lipid levels or normal plasma HDL levels.

SUMMARY:

We and others have hypothesized that HDL and LDL-derived oxidized phospholipids may be part of a system of nonspecific innate immunity. We therefore propose that determination of HDL capacity against LDL oxidation and the detection of proinflammatory HDL may be a useful marker of susceptibility to atherosclerosis.

PMID:
12151851
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wolters Kluwer
Loading ...
Support Center