Cor Vasa 2006, 48(3):114-120 | DOI: 10.33678/cor.2006.037

Reverse cholesterol transport

Ivana Králová Lesná^*, Jan Kovář, Rudolf Poledne

Laboratoř pro výzkum aterosklerózy, Centrum experimentálního výzkumu chorob srdce a cév, Institut klinické a experimentální medicíny, Praha, Česká republika

Reverse cholesterol transport (RCT), i. e., transport of cholesterol from peripheral tissue to the liver, is an important physiological mechanism whereby a major role is played by high-density lipoprotein (HDL) particles. Removal of excess cholesterol from cells is important for maintaining cholesterol homeostasis in cells and occurs via several mechanisms.
Cholesterol is removed from cells actively mainly via membrane proteins called ABCA1 (ATP-binding cassette transporter A1) or ABCG1 and ABCG4 (ATP-binding cassette transporters G1 and G4); additional cholesterol may leave cells via SR-BI (scavenger receptor class B type I) or diffusion. The relative importance of individual receptors depends on their expression and type of the cholesterol acceptor available. Released non-polar cholesterol binds to HDL particles or their precursors, becomes esterified by lecithin: cholesterolacyltransferase (LCAT) to cholesterol esters and subsequently transported to the liver. Part of HDL-cholesterol may be exchanged, in the circulation, for triglycerides from apolipoprotein B-containing lipoproteins via CETP (cholesterol-ester transfer protein) and transported to the liver by these proteins. Another proportion of HDL-cholesterol is selectively uptaken in the liver by hepatic SR-BI. Although the cholesterol released from vascular wall macrophages makes up only a small proportion of total RCT, it has an essential antiatherogenic value. New antiatherogenic strategies are aimed at increasing cholesterol efflux from cells and accelerating RCT. As HDL-cholesterol levels need not necessarily always correlate with their ability to be involved in RCT, it is critical to study in detail the kinetics of individual steps of RCT.

Keywords: Reverse cholesterol transport; HDL; Atherogenesis

Published: March 1, 2006  Show citation