Evidence map›Paper›PMID 21875899›Full record

ReviewHuman molecular genetics2011

Thirty-five common variants for coronary artery disease: the fruits of much collaborative labour.

John F Peden, Martin Farrall

Open access · bronzeAbstract readReview
In one paragraph

Review in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 7 pooled it
12.0field-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

73 citing papers in PubMed, 7 syntheses or guidelines pooled it, 143 citations in OpenAlex.

  1. Pooled it
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  8. Polymorphic and Expressional Analysis of GenesInternational journal of hypertension · 2025
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  14. Aging · 2020
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13 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 1 institution in 1 country.

John F PedenDepartment of Cardiovascular Medicine, The Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford, UK.
Martin Farrall
Centre for Human Genetics · GB

Funding

British Heart FoundationWellcome Trust 090532Wellcome Trust 090532/Z/09/Z
6 · The paper itself

Abstract

Coronary artery disease (CAD) is the leading cause of death worldwide. Affected individuals cluster in families in patterns that reflect the sharing of numerous susceptibility genes. Genome-wide and large-scale gene-centric genotyping studies that involve tens of thousands of cases and controls have now mapped common disease variants to 34 distinct loci. Some coronary disease common variants show allelic heterogeneity or copy number variation. Some of the loci include candidate genes that imply conventional or emerging risk factor-mediated mechanisms of disease pathogenesis. Quantitative trait loci associations with risk factors have been informative in Mendelian randomization studies as well as fine-mapping of causative variants. But, for most loci, plausible mechanistic links are uncertain or obscure at present but provide potentially novel directions for research into this disease's pathogenesis. The common variants explain ~4% of inter-individual variation in disease risk and no more than 13% of the total heritability of coronary disease. Although many CAD genes are presently undiscovered, it is likely that larger collaborative genome-wide association studies will map further common/low-penetrance variants and hoped that low-frequency or rare high-penetrance variants will also be identified in medical resequencing experiments.

Indexed as

Genetic VariationCoronary Artery DiseaseDNA Copy Number VariationsGenome-Wide Association StudyHumansQuantitative Trait Loci

Identifiers

PMID21875899
PMCPMC3179381
OpenAlexW2127732764

What OpenQuestion holds

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LicenceCC BY-NC
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.