Evidence map›Paper›PMID 28777110›Full record

ReviewCurrent opinion in lipidology2017

Time to ditch HDL-C as a measure of HDL function?

Graziella E Ronsein, Jay W Heinecke

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in lipidology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  4. Trial
  5. Review
  6. Article
  7. Article
  8. Using heparan sulfate octadecasaccharide (18-mer) as a multi-target agent to protect against sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  9. Oxidative modification of HDL by lipid aldehydes impacts HDL function.Archives of biochemistry and biophysics · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Trends in Serum Lipid Profiles Among Korean Adolescents, 2007-2018.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021
    Article
  17. Article
  18. Article
  19. Article
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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

2 authors at 2 institutions in 2 countries.

Graziella E RonseinaDepartamento de Bioquímica, Instituto de Química, Universidade de São Paulo, Brazil bDepartment of Medicine, University of Washington, Seattle, Washington, USA.
Jay W Heinecke
Universidade de São Paulo · BRUniversity of Washington · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1986 to 2026
$41.4M
Structural Determinants Of Ceruloplasmin Inflammatory ActivityP01HL076491 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI PLOW, EDWARD FRANKLIN · 2004 to 2019
$27.3M
Role of Serum Amyloid A in Diabetic Vascular DiseaseP01HL092969 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 2008 to 2019
$23.5M
CARDIOVASCULAR RESEARCH TRAINING PROGRAMT32HL007828 · NHLBI · UNIVERSITY OF WASHINGTON · PI Francis Kim, Farid Moussavi-Harami · 1997 to 2026
$10.2M
Quantitative Assessment of HDL FunctionR01HL112625 · NHLBI · UNIVERSITY OF WASHINGTON · PI HEINECKE, JAY W · 2012 to 2016
$2.1M
Cardioprotective Mechanisms of HDLR01HL108897 · NHLBI · UNIVERSITY OF WASHINGTON · PI HEINECKE, JAY W · 2012 to 2015
$1.7M
APOC3, HDL Function and Cardiovascular Complications of T1DMDP3DK108209 · NIDDK · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E., HEINECKE, JAY W · 2015 to 2015
$1.6M
NHLBI NIH HHS P01 HL076491NHLBI NIH HHS P01 HL092969NHLBI NIH HHS R01 HL108897NHLBI NIH HHS R01 HL112625NHLBI NIH HHS T32 HL007828NIDDK NIH HHS DP3 DK108209NIDDK NIH HHS P30 DK017047
6 · The paper itself

Abstract

purpose of reviewEpidemiological and clinical studies link low levels of HDL cholesterol (HDL-C) with increased risk of atherosclerotic cardiovascular disease (CVD). However, genetic polymorphisms linked to HDL-C do not associate consistently with CVD risk, and randomized clinical studies of drugs that elevate HDL-C via different mechanisms failed to reduce CVD risk in statin-treated patients with established CVD. New metrics that capture HDL's proposed cardioprotective effects are therefore urgently needed. RECENT

findingsRecent studies demonstrate cholesterol efflux capacity (CEC) of serum HDL (serum depleted of cholesterol-rich atherogenic lipoproteins) is an independent and better predictor of incident and prevalent CVD risk than HDL-C. However, it remains unclear whether therapies that increase CEC are cardioprotective. Other key issues are the impact of HDL-targeted therapies on HDL particle size and concentration and the relationship of those changes to CEC and cardioprotection. SUMMARY: It is time to end the clinical focus on HDL-C and to understand how HDL's function, protein composition and size contribute to CVD risk. It will also be important to link variations in function and size to HDL-targeted therapies. Developing new metrics for quantifying HDL function, based on better understanding HDL metabolism and macrophage CEC, is critical for achieving these goals.

Indexed as

AnimalsBiomarkersCholesterol, HDLHumansBiomarkersCholesterol, HDL

Identifiers

PMID28777110
PMCPMC5659345
OpenAlexW2744983506

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.