Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3275137 | Médecine des Maladies Métaboliques | 2009 | 5 Pages |
Abstract
Decreased HDL-cholesterol plasma levels represent the major risk factor associated with coronary atherosclerosis progression. Classically, the atheroprotective mechanism of HDL is thought to be related to its role in reverse transport of cholesterol from peripheral tissues to the liver. Recent studies indicate that endothelium is a key target of HDL action. HDL stimulates endothelial nitric oxide synthase (eNOS), and the nitric oxide (NO) produced by eNOS regulates blood flow. HDL also protects endothelial cells from apoptosis and promotes their growth and their migration. Moreover, HDL has antiinflammatory and antithrombotic actions. Thus, in addition to its cholesterol-transporting properties, HDL favourably regulates endothelial cell phenotype and reduces the risk of thrombosis. The antiatherogenic action of HDL is also ascribed to its effect to protect LDL from oxidation through HDL-associated enzymes.
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Authors
M.-C. Brindisi, L. Perségol, L. Duvillard, B. Vergès,