J. Lipid Res.  Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on November 1, 2004

Papers In Press, published online ahead of print September 1, 2004
J. Lipid Res., doi:10.1194/jlr.R400007-JLR200
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Submitted on July 20, 2004
Revised on September 1, 2004
Accepted on August 24, 2004

What can we expect from inhibition of CETP activity in the treatment of dyslipidemia?

Greetje J. De Grooth, Anke H. E. M. Klerkx, Erik S. G. Stroes, Anton F. H. Stalenhoef, John J. P. Kastelein, and Jan Albert Kuivenhoven

Department of Vascular Medicine, Academic Medical Center, Amsterdam, Amsterdam 1105AZ

Corresponding Author: j.a.kuivenhoven{at}amc.uva.nl

Although the atheroprotective role of HDL cholesterol (HDL-c) is well-documented, effective therapeutics to selectively increase plasma HDL-c levels are not yet available. Recent progress in unravelling human HDL metabolism has fuelled the development of strategies to decrease the incidence and progression of coronary artery disease (CAD) by raising HDL-c. In this quest for novel drugs, cholesteryl ester transfer protein (CETP) represents a pivotal target. The role of this plasma protein in HDL metabolism is highlighted by the discovery that genetic CETP deficiency is the main cause of extremely high HDL-c levels in Asian populations. The use of CETP inhibitors to effectively increase HDL-c concentration in humans was recently published and data with regard to the effect on human atherosclerosis are expected shortly. This review discusses the potential of CETP inhibitors to protect against atherosclerosis in the context of the current knowledge of CETP function in both rodents and man.


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