Evidence mapPaperPMID 24385513Full record

ReviewCirculation research2014

High-density lipoprotein and atherosclerosis regression: evidence from preclinical and clinical studies.

Jonathan E Feig, Bernd Hewing, Jonathan D Smith, Stanley L Hazen, Edward A Fisher

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 2 pooled it
21.1field-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

83 citing papers in PubMed, 2 syntheses or guidelines pooled it, 172 citations in OpenAlex.

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23 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

5 authors at 1 institution in 1 country.

Jonathan E FeigFrom the Departments of Medicine (Cardiology) and Cell Biology, Marc and Ruti Bell Vascular Biology Program, New York University School of Medicine, New York, NY (J.E.F., B.H., E.A.F.); and Department of Cellular and Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Cleveland, OH (J.D.S., S.L.H.). J.E.F. is currently affiliated with Department of Medicine (Cardiology), Mount Sinai School of Medicine, New York, NY. B.H. is currently affiliated with Medizinische Klinik für Kardiologie und Angiologie, Campus Mitte, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Bernd Hewing
Jonathan D Smith
Stanley L Hazen
Edward A Fisher
New York College of Health Professions · US

Funding

MEDICAL SCIENTIST TRAININGT32GM007308 · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · 1985 to 2005
$6.9M
NHLBI NIH HHS HL-084312NHLBI NIH HHS HL-098055NHLBI NIH HHS P01 HL098055NHLBI NIH HHS R01 HL084312NIA NIH HHS AG-029748NIA NIH HHS F30 AG029748NIGMS NIH HHS T32 GM007308
6 · The paper itself

Abstract

High-density lipoprotein (HDL) particles transport (among other molecules) cholesterol (HDL-C). In epidemiological studies, plasma HDL-C levels have an inverse relationship to the risk of atherosclerotic cardiovascular disease. It has been assumed that this reflects the protective functions of HDL, which include their ability to promote cholesterol efflux. Yet, several recent pharmacological and genetic studies have failed to demonstrate that increased plasma levels of HDL-C resulted in decreased cardiovascular disease risk, giving rise to a controversy regarding whether plasma levels of HDL-C reflect HDL function, or that HDL is even as protective as assumed. The evidence from preclinical and (limited) clinical studies shows that HDL can promote the regression of atherosclerosis when the levels of functional particles are increased from endogenous or exogenous sources. The data show that regression results from a combination of reduced plaque lipid and macrophage contents, as well as from a reduction in its inflammatory state. Although more research will be needed regarding basic mechanisms and to establish that these changes translate clinically to reduced cardiovascular disease events, that HDL can regress plaques suggests that the recent trial failures do not eliminate HDL from consideration as an atheroprotective agent but rather emphasizes the important distinction between HDL function and plasma levels of HDL-C.

Indexed as

AnimalsAnticholesteremic AgentsAtherosclerosisCholesterol, HDLDisease ProgressionHumansPlaque, AtheroscleroticAnticholesteremic AgentsCholesterol, HDLatherosclerosischolesterol, HDLcoronary artery diseasemiceregression

Identifiers

PMID24385513
PMCPMC3918097
OpenAlexW2531560466

What Socratic 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 Socratic graph.