Evidence map›Paper›PMID 24854407›Full record

ReviewNature reviews. Drug discovery2014

HDL-targeted therapies: progress, failures and future.

Bronwyn A Kingwell, M John Chapman, Anatol Kontush, Norman E Miller

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Drug discovery, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

161 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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  16. Apolipoprotein A (ApoA) in Neurological Disorders: Connections and Insights.International journal of molecular sciences · 2025
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101 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.

Bronwyn A KingwellBaker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia.
M John ChapmanINSERM UMRS-939, Dyslipidemia and Atherosclerosis Research Unit, Pitié-Salpetriere Hospital, Université Pierre et Marie Curie, Paris 6, France.
Anatol KontushINSERM UMRS-939, Dyslipidemia and Atherosclerosis Research Unit, Pitié-Salpetriere Hospital, Université Pierre et Marie Curie, Paris 6, France.
Norman E MillerMagdalen College, University of Oxford, Oxford OX1 4AU, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since the discovery in the 1970s that plasma levels of high-density lipoprotein cholesterol (HDL-C) are inversely associated with cardiovascular outcome, it has been postulated that HDL is anti-atherogenic and that increasing HDL-C levels is a promising therapeutic strategy. However, the recent failure of three orally active, HDL-C-raising agents has introduced considerable controversy, prompting the question of whether increasing the cholesterol cargo of HDL in a non-selective manner is an effective pharmacological approach for the translation of its atheroprotective and vasculoprotective activities. The interrelationships between HDL-C concentration, HDL particle number and levels of diverse HDL particle subpopulations of defined composition are complex, as are their relationships with reverse cholesterol transport and other anti-atherogenic functions. Such complexity highlights the incompleteness of our understanding of the biology of HDL particles. This article examines the HDL hypothesis in molecular and mechanistic terms, focusing on features that have been addressed, those that remain to be tested, and potential new targets for future pharmacological interventions.

Indexed as

Clinical Trials as TopicModels, BiologicalMolecular Targeted TherapyAnimalsApolipoprotein A-ICardiovascular DiseasesCholesterol Ester Transfer ProteinsDrugs, InvestigationalHumansHypolipidemic AgentsLipoproteins, HDLNiacinPhosphatidylcholine-Sterol O-AcyltransferaseRecombinant ProteinsUp-RegulationAPOA1 protein, humanApolipoprotein A-ICETP protein, humanCholesterol Ester Transfer ProteinsDrugs, InvestigationalHypolipidemic AgentsLipoproteins, HDLNiacinPhosphatidylcholine-Sterol O-AcyltransferaseRecombinant Proteins

Identifiers

PMID24854407

What Socratic holds

Texttitle and abstract
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.