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Regulation of reverse cholesterol transport and clinical implications

Authors
Journal
The American Journal of Cardiology
0002-9149
Publisher
Elsevier
Publication Date
Volume
92
Issue
4
Identifiers
DOI: 10.1016/s0002-9149(03)00615-5
Disciplines
  • Biology
  • Medicine

Abstract

Abstract Plasma levels of high-density lipoprotein (HDL) cholesterol and its major protein, apolipoprotein A-I, are inversely correlated with the incidence of atherosclerotic cardiovascular disease. Low HDL cholesterol and apolipoprotein A-I levels often are found in association with other cardiovascular risk factors, including the metabolic syndrome, insulin resistance, and type 2 diabetes mellitus. However, overexpression of apolipoprotein A-I in animals has been shown to reduce progression and even induce regression of atherosclerosis, indicating that apolipoprotein A-I is directly protective against atherosclerosis. A major mechanism by which apolipoprotein A-I inhibits atherosclerosis may be by promoting cholesterol efflux from macrophages and returning it to the liver for excretion, a process termed reverse cholesterol transport. This article focuses on new developments in the regulation of reverse cholesterol transport and the clinical implications of those developments.

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