Evidence map›Paper›PMID 21304474›Full record

ReviewNature reviews. Cardiology2011

HDL and cardiovascular disease: atherogenic and atheroprotective mechanisms.

Mohamad Navab, Srinivasa T Reddy, Brian J Van Lenten, Alan M Fogelman

Abstract readReview
PubMed Publisher
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 325 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
325citing papers in PubMed, 1 pooled it
52.2field-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

325 citing papers in PubMed, 1 synthesis or guideline pooled it, 659 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Article
  7. Early atherogenesis: In search of etiology.International journal of cardiology. Cardiovascular risk and prevention · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Reduced antioxidant high-density lipoprotein function in heart failure with preserved ejection fraction.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
    Observational
  18. Observational
  19. Article
  20. Article

265 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 at 1 institution in 1 country.

Mohamad NavabDepartment of Medicine, David Geffen School of Medicine, UCLA, 10833 Le Conte Avenue, Los Angeles, CA 90095-1679, USA. mnavab@mednet.ucla.edu
Srinivasa T Reddy
Brian J Van Lenten
Alan M Fogelman
University of California, Los Angeles · US

Funding

ULTRASTRUCTURE OF THE INTIMA IN EARLY LESION FORMATIONP01HL030568 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FOGELMAN, ALAN M · 1985 to 2019
$55.2M
NHLBI NIH HHS HL 30568
6 · The paper itself

Abstract

The lipoprotein HDL has two important roles: first, it promotes reverse cholesterol transport, and second, it modulates inflammation. Epidemiological studies show that HDL-cholesterol levels are inversely correlated with the risk of cardiovascular events. However, many patients who experience a clinical event have normal, or even high, levels of HDL cholesterol. Measuring HDL-cholesterol levels provides information about the size of the HDL pool, but does not predict HDL composition or function. The main component of HDL, apolipoprotein A-I (apo A-I), is largely responsible for reverse cholesterol transport through the macrophage ATP-binding cassette transporter ABCA1. Apo A-I can be damaged by oxidative mechanisms, which render the protein less able to promote cholesterol efflux. HDL also contains a number of other proteins that are affected by the oxidative environment of the acute-phase response. Modification of the protein components of HDL can convert it from an anti-inflammatory to a proinflammatory particle. Small peptides that mimic some of the properties of apo A-I have been shown in preclinical models to improve HDL function and reduce atherosclerosis without altering HDL-cholesterol levels. Robust assays to evaluate the function of HDL are needed to supplement the measurement of HDL-cholesterol levels in the clinic.

Indexed as

Apolipoprotein A-ICardiovascular DiseasesCholesterol, HDLCholesterol, LDLHumansInflammationOxidative StressRisk AssessmentRisk FactorsApolipoprotein A-ICholesterol, HDLCholesterol, LDL

Identifiers

PMID21304474
OpenAlexW2042344342

What OpenQuestion holds

Textmetadata
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.