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STATE-OF-THE-ART PAPER

High-Density Lipoprotein Function

Recent Advances

Atherosclerosis Research Unit, Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California

Manuscript received April 24, 2005; revised manuscript received May 29, 2005, accepted June 7, 2005.

^_* Reprint requests and correspondence: Dr. Gregg C. Fonarow, 47-123 CHS, 10833 LeConte Avenue, Los Angeles, California 90095 (Email: gfonarow{at}mednet.ucla.edu).

Although high-density lipoproteins (HDL) possess many features that contribute to the association between elevated HDL cholesterol and protection from atherosclerosis, these lipoproteins may be modified in certain individuals and/or circumstances to become proinflammatory. The ability of HDL to inhibit or paradoxically to enhance vascular inflammation, lipid oxidation, plaque growth, and thrombosis reflects changes in specific enzyme and protein components. The anti-inflammatory and proinflammatory functional properties of HDL can now be assessed using cell-based and cell-free assays. Acute or chronic systemic inflammation and the metabolic syndrome appear to render HDL proinflammatory. In contrast, statins and experimental agents such as apolipoprotein A-1 mimetics render HDL more anti-inflammatory. Functional characterization of HDL is a promising method for enhanced assessment of cardiovascular risk and effectiveness of risk reduction.

Abbreviations and Acronyms   ABCA1 = adenosine triphosphate-binding cassette transporter A1   apoA-1 = apolipoprotein A-1   CETP = cholesteryl ester transfer protein   CFA = cell-free assay   CHD = coronary heart disease   HDL = high-density lipoprotein   HDL-C = high-density lipoprotein cholesterol   LDL = low-density lipoprotein   MCA = monocyte chemotaxis assay   MCP = monocyte chemotaxis protein   ox-LDL = oxidized low-density lipoprotein

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