Evidence map›Paper›PMID 22480919›Full record

ReviewTrends in genetics : TIG2012

Genetics of atherosclerosis.

Aldons J Lusis

Abstract readReview
In one paragraph

Review in Trends in genetics : TIG, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing 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

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

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Early atherogenesis: In search of etiology.International journal of cardiology. Cardiovascular risk and prevention · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Residual risks and evolving atherosclerotic plaques.Molecular and cellular biochemistry · 2023
    Review
  14. A PolynesianHGG advances · 2023
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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

1 author.

Aldons J LusisUniversity of California, Los Angeles, Department of Medicine/Division of Cardiology, Los Angeles, CA 90095-1679, USA. jlusis@mednet.ucla.edu

Funding

ULTRASTRUCTURE OF THE INTIMA IN EARLY LESION FORMATIONP01HL030568 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FOGELMAN, ALAN M · 1985 to 2019
$55.2M
Systems genomics of metabolic syndrome traitsP01HL028481 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 1985 to 2019
$50.2M
Systems Genetics of Type 1 Diabetes ComplicationsDP3DK094311 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2011 to 2011
$4.3M
Dissection of HDL function using mouse modelsR01HL094322 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2009 to 2013
$1.9M
DNA methylation and its relationship to gene expression and physiologic traitsR01GM095656 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PELLEGRINI, MATTEO · 2011 to 2014
$1.8M
A Systems Approach to Uncover Novel Genes and Networks in Heart FailureR21HL110667 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE, WANG, YIBIN · 2011 to 2012
$424k
NCCDPHP CDC HHS DP3 D094311NHLBI NIH HHS P01 HL028481NHLBI NIH HHS P01 HL030568NHLBI NIH HHS P01 HL28481NHLBI NIH HHS P01 HL305685NHLBI NIH HHS R01 HL094322NHLBI NIH HHS R01 HL0943221NHLBI NIH HHS R21 HL110667NHLBI NIH HHS R21 HL110667-01NIDDK NIH HHS DP3 DK094311NIGMS NIH HHS 1R01 GM0956561NIGMS NIH HHS R01 GM095656
6 · The paper itself

Abstract

Genome-wide association studies (GWAS) from the past several years have provided the first unbiased evidence of the genes contributing to common cardiovascular disease traits in European and some Asian populations. The results not only confirmed the importance of prior knowledge, such as the central role of lipoproteins, but also revealed that there is still much to learn about the underlying mechanisms of this disease, as most of the associated genes do not appear to be involved in pathways previously connected to atherosclerosis. In this review, I focus on the common forms of the disease and look at both human and animal model studies. I summarize what was known before GWAS, highlight how the field has been changed by GWAS, and discuss future considerations, such as the limitations of GWAS and strategies that may lead to a more complete, mechanistic understanding of atherosclerosis.

Indexed as

AnimalsAtherosclerosisCoronary Artery DiseaseGenome-Wide Association StudyHumansQuantitative Trait LociRisk Factors

Identifiers

PMID22480919
PMCPMC3362664

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.