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Cited by 870

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Cholesteryl Ester Transfer Protein: A Novel Target for Raising HDL and Inhibiting Atherosclerosis

Barter, Philip J., Brewer, H. Bryan, Chapman, M. John, Hennekens, Charles H., Rader, Daniel J., Tall, Alan R.·2003·Arteriosclerosis, Thrombosis, and Vascular Biology

Abstract

Cholesteryl ester transfer protein (CETP) promotes the transfer of cholesteryl esters from antiatherogenic HDLs to proatherogenic apolipoprotein B (apoB)–containing lipoproteins, including VLDLs, VLDL remnants, IDLs, and LDLs. A deficiency of CETP is associated with increased HDL levels and decreased LDL levels, a profile that is typically antiatherogenic. Studies in rabbits, a species with naturally high levels of CETP, support the therapeutic potential of CETP inhibition as an approach to retarding atherogenesis. Studies in mice, a species that lacks CETP activity, have provided mixed results. Human subjects with heterozygous CETP deficiency and an HDL cholesterol level >60 mg/dL have a reduced risk of coronary heart disease. Evidence that atherosclerosis may be increased in CETP-deficient subjects whose HDL levels are not increased is difficult to interpret and may reflect confounding or bias. Small-molecule inhibitors of CETP have now been tested in human subjects and shown to increase the concentration of HDL cholesterol while decreasing that of LDL cholesterol and apoB. Thus, it seems important and timely to test the hypothesis in randomized trials of humans that pharmacological inhibition of CETP retards the development of atherosclerosis.

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Crossref · 10.1161/01.atv.0000054658.91146.64

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Metadata

Authors
Barter, P. J., Brewer, H. B., Chapman, M. J., Hennekens, C. H., Rader, D. J., & Tall, A. R.
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Published
2003-02
Volume
23
Issue
2
Pages
160-167
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
OpenAlex
W2148609678
Cited by
870
References
3
FWCI
51.08
Type
journal article
Language
en
Open access
closed

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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