HDL biology
A review names CETP, apoA-II, and hepatic lipase as prime targets for pharmacologic inhibition among new HDL-directed atherosclerosis therapies (Curr Atheroscler Rep 2000)
Original title: High-density lipoprotein metabolism: molecular targets for new therapies for atherosclerosis
This review discusses genes involved in HDL metabolism as potential targets for new atherosclerotic cardiovascular disease therapies, noting that because HDL metabolism is dynamic, the effect of an HDL-oriented intervention on atherosclerosis cannot necessarily be predicted from its effect on plasma HDL cholesterol level. Based on animal model data, candidates for pharmacologic upregulation, infusion, or overexpression include apolipoprotein A-I, apoE, apoA-IV, lipoprotein lipase, ATP-binding cassette protein 1, lecithin cholesterol acyltransferase, and scavenger receptor B-I. In contrast, apoA-II, cholesteryl ester transfer protein (CETP), and hepatic lipase are identified as candidates for inhibition. The authors anticipate the next decade will bring a transition from preclinical studies to clinical trials of new HDL-targeted atherosclerosis therapies.
Original abstract
New therapeutic approaches to the prevention and treatment of atherosclerotic cardiovascular disease (ASCVD) are needed. Plasma levels of high-density lipoprotein (HDL) cholesterol are inversely associated with risk of ASCVD. Genes involved in the metabolism of HDL represent potential targets for the development of such therapies. Because HDL metabolism is a dynamic process, the effect of a specific HDL-oriented intervention on atherosclerosis cannot necessarily be predicted by its effect on the plasma HDL cholesterol level. Based on available data in animal models, some gene products are candidates for pharmacologic upregulation, infusion, or overexpression, including apolipoprotein (apo)A-I, apoE, apoA-IV, lipoprotein lipase (LPL), ATP-binding cassette protein 1 (ABC1), lecithin cholesterol acyltransferase (LCAT), and scavenger receptor B-I (SR-BI). In contrast, some gene products are potential candidates for inhibition, including apoA-II, cholesteryl ester transfer protein (CETP), and hepatic lipase. The next decade will witness the transition from preclinical studies to clinical trials of a variety of new therapies targeted toward HDL metabolism and atherosclerosis.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.