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CETP and atherosclerosis.

Ever since cholesteryl ester transfer protein (CETP) was first identified, there have been conflicting opinions regarding its role (if any) in the development of atherosclerosis. According to 1 view, CETP is antiatherogenic by virtue of its ability to increase the rate of reverse cholesterol transport (RCT), the pathway in which cholesterol in peripheral tissues is transported to the liver for elimination in bile. This pathway involves an initial uptake of cell cholesterol by HDL, where it is esterified before being transferred by CETP to LDL and VLDL. The cholesteryl esters in the VLDL/LDL pool are subsequently delivered to the liver and ultimately eliminated from the body as a component of bile. Thus, to the extent that CETP enhances the rate of RCT, it may be an antiatherogenic factor. However, the fact that CETP redistributes cholesteryl esters from the nonatherogenic HDL to the potentially atherogenic VLDL/LDL implies that it may also be proatherogenic.

The situation is even further complicated by mounting evidence that concentration-dependent, anti-inflammatory functions of HDL may also contribute to its antiatherogenicity.1 Because CETP decreases the concentration of HDL,2 it may decrease the anti-inflammatory impact of this lipoprotein fraction in a process that is ultimately proatherogenic. Thus, on theoretical grounds, CETP may be either proatherogenic or antiatherogenic, depending on which of the HDL functions is dominant. As outlined below, the situation has not been clarified by more direct studies in vivo in animals in which evidence supporting both a proatherogenic3 4 5 and an antiatherogenic6 7 role of CETP has been reported.

CETP is a hydrophobic glycoprotein that is secreted from the liver and that circulates in plasma, bound mainly to HDL.8 It promotes the redistribution of cholesteryl esters, triglyceride, and, to a lessor extent, phospholipids between plasma lipoproteins. CETP picks up lipids from …