Evidence map›Paper›PMID 22517614›Full record

ReviewCurrent opinion in lipidology2012

Rationale for cholesteryl ester transfer protein inhibition.

Bernd Hewing, Edward A Fisher

Abstract readReview
In one paragraph

Review in Current opinion in lipidology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
9.4field-weighted citation impact, top 2% 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

25 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Observational
  12. Article
  13. Article
  14. Review
  15. A coding variant in SR-BI (I179N) significantly increases atherosclerosis in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2013
    Article
  16. Article
  17. Article
  18. Article
  19. HDL--is it too big to fail?Nature reviews. Endocrinology · 2013
    Review
  20. Review
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

2 authors at 2 institutions in 2 countries.

Bernd HewingDivision of Cardiology (Preventive Cardiology), Department of Medicine, New York University School of Medicine, New York, New York 10016, USA.
Edward A Fisher
Charité - Universitätsmedizin Berlin · DEGTx (United States) · US

Funding

Regression of Atherosclerosis CoreP01HL098055 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI FISHER, EDWARD A · 2010 to 2014
$12.1M
Molecular Regulation of Atherosclerosis Regression - RenewalR01HL084312 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A · 2006 to 2024
$11.4M
NHLBI NIH HHS HL084312NHLBI NIH HHS HL098055NHLBI NIH HHS P01 HL098055NHLBI NIH HHS R01 HL084312
6 · The paper itself

Abstract

purpose of reviewRaising HDL cholesterol (HDL-C) has become an attractive therapeutic target to lower cardiovascular risk in addition to statins. Inhibition of the cholesteryl ester transfer protein (CETP), which mediates the transfer of cholesteryl esters from HDL to apolipoprotein B-containing particles, leads to a substantial increase in HDL-C levels. Various CETP inhibitors are currently being evaluated in phase II and phase III clinical trials. However, the beneficial effect of CETP inhibition on cardiovascular outcome remains to be established. RECENT

findingsTorcetrapib, the first CETP inhibitor tested in a phase III clinical trial (ILLUMINATE), failed in 2006 because of an increase in all-cause mortality and cardiovascular events that subsequently were attributed to nonclass-related off-target effects (particularly increased blood pressure and low serum potassium) related to the stimulation of aldosterone production. Anacetrapib, another potent CETP inhibitor, raises HDL-C levels by approximately 138% and decreases LDL cholesterol (LDL-C) levels by approximately 40%, without the adverse off-targets effects of torcetrapib (DEFINE study). The CETP modulator dalcetrapib raises HDL-C levels by approximately 30% (with only minimal effect on LDL-C levels) and proved safety in the dal-VESSEL and dal-PLAQUE trials involving a total of nearly 600 patients. Evacetrapib, a relatively new CETP inhibitor, exhibited favorable changes in the lipid profile in a phase II study. SUMMARY: The two ongoing outcome trials, dal-OUTCOMES (dalcetrapib) and REVEAL (anacetrapib), will provide more conclusive answers for the concept of reducing cardiovascular risk by raising HDL-C with CETP inhibition.

Indexed as

AmidesAnimalsBenzodiazepinesCholesterol Ester Transfer ProteinsDrug DiscoveryEstersHumansOxazolidinonesQuinolinesSulfhydryl CompoundsAmidesanacetrapibBenzodiazepinesCholesterol Ester Transfer ProteinsdalcetrapibEstersevacetrapibOxazolidinonesQuinolinesSulfhydryl Compoundstorcetrapib

Identifiers

PMID22517614
PMCPMC3924318
OpenAlexW1973014196

What OpenQuestion holds

Textmetadata
LicenceTDM
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.