Evidence map›Paper›PMID 20556633›Full record

ReviewCellular and molecular life sciences : CMLS2010

Cholesteryl ester transfer protein and its inhibition.

Olaf Weber, Hilmar Bischoff, Carsten Schmeck, Michael-Friedrich Böttcher

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.6field-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

11 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Addressing phenoconversion: the Achilles' heel of personalized medicine.British journal of clinical pharmacology · 2015
    Review
  6. Article
  7. Article
  8. Article
  9. Review
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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

4 authors at 2 institutions in 2 countries.

Olaf WeberBayer Healthcare AG/Bayer Schering Pharma, 42096, Wuppertal, Germany. olaf.weber@bayerhealthcare.com
Hilmar Bischoff
Carsten Schmeck
Michael-Friedrich Böttcher
Bayer (Germany) · DEBayer (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholesteryl ester transfer protein (CETP) is a plasma glycoprotein that facilitates the transfer of cholesteryl esters from the atheroprotective high density lipoprotein (HDL) to the proatherogenic low density lipoprotein cholesterol (LDL) and very low density lipoprotein cholesterol (VLDL) leading to lower levels of HDL but raising the levels of proatherogenic LDL and VLDL. Inhibition of CETP is considered a potential approach to treat dyslipidemia. However, discussions regarding the role of CETP-mediated lipid transfer in the development of atherosclerosis and CETP inhibition as a potential strategy for prevention of atherosclerosis have been controversial. Although many animal studies support the hypothesis that inhibition of CETP activity may be beneficial, negative phase III studies on clinical endpoints with the CETP inhibitor torcetrapib challenged the future perspectives of CETP inhibitors as potential therapeutic agents. The review provides an update on current understanding of the molecular mechanisms involved in CETP activity and its inhibition.

Indexed as

Anticholesteremic AgentsAtherosclerosisCholesterol Ester Transfer ProteinsClinical Trials as TopicDrug DesignHumansAnticholesteremic AgentsCholesterol Ester Transfer Proteins

Identifiers

PMID20556633
PMCPMC11115880
OpenAlexW2071087311

What OpenQuestion holds

Textmetadata
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.