Evidence map›Paper›PMID 19825813›Full record

ReviewEuropean heart journal2010

Cholesteryl ester transfer protein: at the heart of the action of lipid-modulating therapy with statins, fibrates, niacin, and cholesteryl ester transfer protein inhibitors.

M John Chapman, Wilfried Le Goff, Maryse Guerin, Anatol Kontush

Open access · bronzeAbstract readReview
In one paragraph

Review in European heart journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 2 pooled it
25.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

102 citing papers in PubMed, 2 syntheses or guidelines pooled it, 294 citations in OpenAlex.

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  7. HDL cholesterol, apolipoproteins, and cardiovascular risk in hemodialysis patients.Journal of the American Society of Nephrology : JASN · 2015
    Trial
  8. The effects of extended release niacin on lipoprotein sub-particle concentrations in HIV-infected patients.Hawai'i journal of medicine & public health : a journal of Asia Pacific Medicine & Public Health · 2013
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  17. Dysfunctional high-density lipoprotein: an updated review.Frontiers in cardiovascular medicine · 2025
    Review
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  19. Article
  20. Article

42 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

M John ChapmanINSERM, UMR S939, Dyslipidemia, Inflammation and Atherosclerosis Research Unit, University Pierre and Marie Curie-Paris 6, Pavillon Benjamin Delessert, Hôpital de la Pitié, 83 Boulevard de l'Hôpital, Paris Cedex 13, France. john.chapman@upmc.fr
Wilfried Le Goff
Maryse Guerin
Anatol Kontush
Inserm · FRCentre de Recherche sur l'Inflammation · FRSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subnormal plasma levels of high-density lipoprotein cholesterol (HDL-C) constitute a major cardiovascular risk factor; raising low HDL-C levels may therefore reduce the residual cardiovascular risk that frequently presents in dyslipidaemic subjects despite statin therapy. Cholesteryl ester transfer protein (CETP), a key modulator not only of the intravascular metabolism of HDL and apolipoprotein (apo) A-I but also of triglyceride (TG)-rich particles and low-density lipoprotein (LDL), mediates the transfer of cholesteryl esters from HDL to pro-atherogenic apoB-lipoproteins, with heterotransfer of TG mainly from very low-density lipoprotein to HDL. Cholesteryl ester transfer protein activity is elevated in the dyslipidaemias of metabolic disease involving insulin resistance and moderate to marked hypertriglyceridaemia, and is intimately associated with premature atherosclerosis and high cardiovascular risk. Cholesteryl ester transfer protein inhibition therefore presents a preferential target for elevation of HDL-C and reduction in atherosclerosis. This review appraises recent evidence for a central role of CETP in the action of current lipid-modulating agents with HDL-raising potential, i.e. statins, fibrates, and niacin, and compares their mechanisms of action with those of pharmacological agents under development which directly inhibit CETP. New CETP inhibitors, such as dalcetrapib and anacetrapib, are targeted to normalize HDL/apoA-I levels and anti-atherogenic activities of HDL particles. Further studies of these CETP inhibitors, in particular in long-term, large-scale outcome trials, will provide essential information on their safety and efficacy in reducing residual cardiovascular risk.

Indexed as

Cardiovascular AgentsCardiovascular DiseasesCholesterolCholesterol Ester Transfer ProteinsCholesterol, HDLFibric AcidsHumansHydroxymethylglutaryl-CoA Reductase InhibitorsHypolipidemic AgentsNiacinCardiovascular AgentsCETP protein, humanCholesterolCholesterol Ester Transfer ProteinsCholesterol, HDLFibric AcidsHydroxymethylglutaryl-CoA Reductase InhibitorsHypolipidemic AgentsNiacin

Identifiers

PMID19825813
PMCPMC2806550
OpenAlexW2064366700

What OpenQuestion holds

Texttitle and abstract
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.