Evidence map›Paper›PMID 25410905›Full record

ReviewMolecules and cells2014

Cholesteryl ester transfer protein (CETP) deficiency and CETP inhibitors.

Hiroshi Mabuchi, Atsushi Nohara, Akihiro Inazu

Open access · diamondAbstract readReview
In one paragraph

Review in Molecules and cells, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
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  4. 2025 Egyptian guidelines for the management of dyslipidemia.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2026
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  17. TheFrontiers in aging neuroscience · 2022
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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

3 authors at 1 institution in 1 country.

Hiroshi MabuchiDepartment of Lipidology, Graduate School of Medical Science, Kanazawa University, Kanazawa 920-8640, Japan.
Atsushi NoharaDepartment of Lipidology, Graduate School of Medical Science, Kanazawa University, Kanazawa 920-8640, Japan.
Akihiro InazuLaboratory Science, Graduate School of Medical Science, Kanazawa University, Kanazawa 920-8640, Japan.
Kanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidemiologic studies have shown that low-density lipoprotein cholesterol (LDL-C) is a strong risk factor, whilst high-density lipoprotein cholesterol (HDL-C) reduces the risk of coronary heart disease (CHD). Therefore, strategies to manage dyslipidemia in an effort to prevent or treat CHD have primarily attempted at decreasing LDL-C and raising HDL-C levels. Cholesteryl ester transfer protein (CETP) mediates the exchange of cholesteryl ester for triglycerides between HDL and VLDL and LDL. We have published the first report indicating that a group of Japanese patients who were lacking CETP had extremely high HDL-C levels, low LDL-C levels and a low incidence of CHD. Animal studies, as well as clinical and epidemiologic evidences, have suggested that inhibition of CETP provides an effective strategy to raise HDL-C and reduce LDL-C levels. Four CETP inhibitors have substantially increased HDL-C levels in dyslipidemic patients. This review will discuss the current status and future prospects of CETP inhibitors in the treatment of CHD. At present anacetrapib by Merck and evacetrapib by Eli Lilly are under development. By 100mg of anacetrapib HDL-C increased by 138%, and LDL-C decreased by 40%. Evacetrapib 500 mg also showed dramatic 132% increase of HDL-C, while LDL-C decreased by 40%. If larger, long-term, randomized, clinical end point trials could corroborate other findings in reducing atherosclerosis, CETP inhibitors could have a significant impact in the management of dyslipidemic CHD patients. Inhibition of CETP synthesis by antisense oligonucleotide or small molecules will produce more similar conditions to human CETP deficiency and may be effective in reducing atherosclerosis and cardiovascular events. We are expecting the final data of prospective clinical trials by CETP inhibitors in 2015.

Indexed as

AnimalsAtherosclerosisBenzodiazepinesCholesterolCholesterol Ester Transfer ProteinsClinical Trials as TopicCoronary DiseaseHumansLipid Metabolism, Inborn ErrorsOxazolidinonesanacetrapibBenzodiazepinesCETP protein, humanCholesterolCholesterol Ester Transfer ProteinsevacetrapibOxazolidinonesCETP deficiencycholesteryl ester transfer protein (CETP)HDL & LDLhyper-HDL-cholesterolemiainhibitors of CETP

Identifiers

PMID25410905
PMCPMC4255097
OpenAlexW2010893377

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.