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(Circulation Research. 2003;92:258.)
© 2003 American Heart Association, Inc.

Editorials

Cardioprotection With High-Density Lipoproteins

Fact or Fiction?

Dipak K. Das

From the Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, Conn.

Correspondence to Dipak K. Das, PhD, Cardiovascular Research Center, University of Connecticut, School of Medicine, Farmington, CT 06030-1110. E-mail ddas@neuron.uchc.edu

Key Words: adhesion molecules • cytokines • tumor necrosis factor • sphingosine • high-density lipoproteins

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Epidemiological studies strongly suggest an inverse correlation between plasma high-density lipoprotein (HDL) concentration and the risk of ischemic heart disease.^1,2 Experimental evidence also exists to indicate cardioprotective effects of HDL.³ However, the mechanism for protective effect of HDL against ischemic heart disease is not completely understood. Although the widely accepted mechanism comprises the ability of HDL to enhance reverse cholesterol transport,⁴ cholesterol-independent mechanisms have also been postulated. For example, lower HDL is associated with endothelial cell injury, which is involved both in the progression of atherogenesis and myocardial ischemia-reperfusion injury. The ability of HDL to inhibit endothelial adhesion molecule expression⁵ and to potentiate prostacyclin release from the endothelial cells⁶ further supports cholesterol-independent mechanism of HDL.

Antiatherogenic property of HDL is mediated by its ability to release cholesterol from lipid-containing cells followed by esterification through lecithin:cholesterol acyltransferase and delivery to the liver and to steroidogenic organs for subsequent synthesis of bile acids and lipoproteins.⁷ Most importantly, HDL can inhibit oxidation of low-density lipoprotein (LDL) as well as the atherogenic effects of oxidized LDL by virtue of its antioxidant property.

Atherosclerosis is an inflammatory disease characterized by adhesion of circulating monocytes to activated endothelial cells followed by migration to the subendothelium with the help of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin.⁸ Consistent with these reports, there is an increased expression of adhesion molecules in atherosclerotic plaque⁹ and upregulation of adhesion molecules in the acute thrombotic process.¹⁰ Recently, an increased plasma concentration of soluble adhesion molecules has been . . . [Full Text of this Article]

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