HDL biology
A Tall-lab review reconciles CETP deficiency and CETP overexpression both showing antiatherogenic signals, via its role in reverse cholesterol transport (Curr Opin Lipidol 1995)
Original title: Cholesteryl ester transfer proteins, reverse cholesterol transport, and atherosclerosis
This review examines the central role of plasma CETP in lipoprotein metabolism through exchange of cholesteryl esters for triglycerides. Human genetic CETP deficiency is associated with increased HDL cholesterol, while CETP overexpression in transgenic mice decreases HDL cholesterol, leading to the proposal that CETP deficiency is antiatherogenic. However, recent observations in both human CETP deficiency and CETP transgenic mice also suggest antiatherogenic effects from CETP expression itself, likely reflecting its role in reverse cholesterol transport. The authors thus highlight an apparent paradox in which both the presence and absence of CETP have been linked to antiatherogenic effects.
Original abstract
Plasma cholesteryl ester transfer protein plays a central role in lipoprotein metabolism by exchanging cholesteryl esters with triglycerides. Human genetic deficiency is associated with increased HDL-cholesterol levels, whereas cholesteryl ester transfer protein overexpression in transgenic mice results in decreased HDL-cholesterol. Thus, it has been proposed that cholesteryl ester transfer protein deficiency is an antiatherogenic state. However, recent observations in human cholesteryl ester transfer protein deficiency and cholesteryl ester transfer protein transgenic mice also suggest antiatherogenic effects of the expression of this protein, probably reflecting its role in reverse cholesterol transport.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.