| Cholesteryl Ester Transfer Protein Inhibition in Cardiovascular Risk Management: Ongoing Trials will End the Confusion. | |
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MedLine Citation:
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PMID: 20645987 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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As delineated in this review, cholesteryl ester transfer protein (CETP) contributes to an atherogenic lipoprotein profile by redistributing cholesteryl esters from high density lipoprotein (HDL) toward apolipoprotein B-containing lipoproteins, especially when the concentration of acceptor triglyceride-rich lipoproteins is elevated. However, this lipid transfer protein may have antiatherogenic proprerties as well. Experimental evidence is accumulating which suggests that the atheroprotective reverse cholesterol transport pathway, whereby cholesterol is removed from peripheral macrophages to the liver for metabolism and biliary excretion, is stimulated by CETP in vivo. CETP could also play a role in host defense against infection and inflammatory processes. Moreover, recently published observational studies show that higher CETP levels may confer cardiovascular protection, whereas reported associations of cardiovascular disease (CVD) with CETP gene variations are equivocal. The concept that HDL cholesterol raising through inhibition of CETP may ameliorate CVD risk has been challenged by the failure of the CETP inhibitor, torcetrapib. Adverse clinical outcome associated with the use of this CETP inhibitor has been attributed to off-target effects, which relate to stimulation of aldosterone. Other CETP inhibitors, such as dalcetrapib and anacetrapib, are unlikely to increase blood pressure. Dalcetrapib is less potent than anacetrapib, which doubles HDL cholesterol. Both inhibitors considerably lower LDL cholesterol.Serious concerns remain about the validity of the concept that HDL cholesterol raising by means of CETP inhibition is a viable strategy. Results of ongoing clinical trials with these drugs will have to be awaited before making up the balance between possible benefits and harms related to pharmacological CETP inhibition. |
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Authors:
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Paul J W H Kappelle; Arie van Tol; Bruce H R Wolffenbuttel; Robin P F Dullaart |
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Publication Detail:
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Type: Journal Article Date: 2010-07-14 |
Journal Detail:
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Title: Cardiovascular therapeutics Volume: 29 ISSN: 1755-5922 ISO Abbreviation: Cardiovasc Ther Publication Date: 2011 Dec |
Date Detail:
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Created Date: 2011-11-28 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101319630 Medline TA: Cardiovasc Ther Country: England |
Other Details:
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Languages: eng Pagination: e89-99 Citation Subset: IM |
Copyright Information:
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© 2010 Blackwell Publishing Ltd. |
Affiliation:
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Department of Endocrinology, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands Department of Cell Biology & Genetics, Erasmus University Medical Center, Rotterdam, The Netherlands. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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