Brief Reviews |
From the Institut für Klinische Chemie und Laboratoriumsmedizin (A.v.E., J.-R.N., G.A.), Zentrallaboratorium, Westfälische Wilhelms-Universität Münster, and the Institut für Arterioskleroseforschung an der Universität Münster (A.v.E., J.-R.N., G.A.), Münster, Germany.
Correspondence to Dr Arnold von Eckardstein, Institut für Klinische Chemie und Laboratoriumsmedizin, Zentrallaboratorium, Westfälische Wilhelms-Universität Münster, Albert-Schweitzer-Strasse 33, D-48129 Münster, Germany. E-mail vonecka{at}uni-muenster.de
AbstractHigh density lipoprotein (HDL) cholesterol is an important risk factor for coronary heart disease, and HDL exerts various potentially antiatherogenic properties, including the mediation of reverse transport of cholesterol from cells of the arterial wall to the liver and steroidogenic organs. Enhancement of cholesterol efflux and of reverse cholesterol transport (RCT) is considered an important target for antiatherosclerotic drug therapy. Levels and composition of HDL subclasses in plasma are regulated by many factors, including apolipoproteins, lipolytic enzymes, lipid transfer proteins, receptors, and cellular transporters. In vitro experiments as well as genetic family and population studies and investigation of transgenic animal models have revealed that HDL cholesterol plasma levels do not necessarily reflect the efficacy and antiatherogenicity of RCT. Instead, the concentration of HDL subclasses, the mobilization of cellular lipids for efflux, and the kinetics of HDL metabolism are important determinants of RCT and the risk of atherosclerosis.
Key Words: apolipoproteins lipid transfer proteins lipases ABC transporter Tangier disease
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