Evidence map›Paper›PMID 21243009›Full record

ReviewNature reviews. Cardiology2011

Novel HDL-directed pharmacotherapeutic strategies.

Emil M Degoma, Daniel J Rader

Abstract readReview
In one paragraph

Review in Nature reviews. Cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
25.3field-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

78 citing papers in PubMed, 148 citations in OpenAlex.

  1. Trial
  2. Radiolabeling lipoproteins to study and manage disease.European journal of nuclear medicine and molecular imaging · 2025
    Review
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  17. The role of monocytosis and neutrophilia in atherosclerosis.Journal of cellular and molecular medicine · 2018
    Review
  18. Article
  19. Article
  20. Article

18 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

2 authors at 2 institutions in 1 country.

Emil M DegomaDivision of Cardiovascular Medicine, University of Pennsylvania, Penn Tower, 6th Floor, 3400 Spruce Street, Philadelphia, PA 19104, USA. emil.degoma@uphs.upenn.edu
Daniel J Rader
University of Pennsylvania · USUniversity of Pennsylvania Health System · US

Funding

INSTITUTIONAL CLINICAL AND TRANSLATIONAL SCIENCE AWARDUL1RR024134 · NCRR · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 2006 to 2011
$70.4M
Institutional Clinical and Translational Science AwardUL1TR000003 · NCATS · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 2012 to 2015
$38.9M
TISSUE CULTURE CORE LABORATORYP01HL022633 · NHLBI · MCP HAHNEMANN UNIVERSITY · PI DE LA LLERA-MOYA, MARGARITA E · 1985 to 2013
$26.1M
Oxidative Modifications of Proteins and Fibrinogen in AtherosclerosisP50HL070128 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 2002 to 2006
$10.8M
Research career training in vascular medicineK12HL083772 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI MOHLER, EMILE R. · 2007 to 2012
$3.1M
CARDIAC SURGERY &STUNNED MYOCARDIUM: CA2+ &ENERGETICSF32HL008377 · NHLBI · CARNEGIE-MELLON UNIVERSITY · PI SOMMERS, KEITH E · 1990 to 1990
–
NCATS NIH HHS UL1 TR000003NCRR NIH HHS UL1 RR024134NCRR NIH HHS UL1-RR‑024134NHLBI NIH HHS HL22633NHLBI NIH HHS K12 HL083772NHLBI NIH HHS K12 HL083772‑01NHLBI NIH HHS P01 HL022633NHLBI NIH HHS P50 HL070128NHLBI NIH HHS P50 HL70128
6 · The paper itself

Abstract

The burden of atherothrombotic cardiovascular disease remains high despite currently available optimum medical therapy. To address this substantial residual risk, the development of novel therapies that attempt to harness the atheroprotective functions of HDL is a major goal. These functions include the critical role of HDL in reverse cholesterol transport, and its anti-inflammatory, antithrombotic, and antioxidant activities. Discoveries in the past decade have shed light on the complex metabolic and antiatherosclerotic pathways of HDL. These insights have fueled the development of HDL-targeted drugs, which can be classified among four different therapeutic approaches: directly augmenting apolipoprotein A-I (apo A-I) levels, such as with apo A-I infusions and upregulators of endogenous apo A-I production; indirectly augmenting apo A-I and HDL-cholesterol levels, such as through inhibition of cholesteryl ester transfer protein or endothelial lipase, or through activation of the high-affinity niacin receptor GPR109A; mimicking the functionality of apo A-I with apo A-I mimetic peptides; and enhancing steps in the reverse cholesterol transport pathway, such as via activation of the liver X receptor or of lecithin-cholesterol acyltransferase.

Indexed as

AnimalsApolipoprotein A-IBiomarkersCardiovascular DiseasesCholesterol, HDLDyslipidemiasHumansHypolipidemic AgentsLipid MetabolismMolecular MimicryTreatment OutcomeAPOA1 protein, humanApolipoprotein A-IBiomarkersCholesterol, HDLHypolipidemic Agents

Identifiers

PMID21243009
PMCPMC3315102
OpenAlexW1984362422

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.