Evidence map›Paper›PMID 17656669›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2007

Genetic susceptibility to peripheral arterial disease: a dark corner in vascular biology.

Joshua W Knowles, Themistocles L Assimes, Jun Li, Thomas Quertermous, John P Cooke

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
6.4field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.

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  16. ADAM12: a genetic modifier of preclinical peripheral arterial disease.American journal of physiology. Heart and circulatory physiology · 2015
    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

5 authors at 1 institution in 1 country.

Joshua W KnowlesFalk Cardiovascular Research Building, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA, 94305-5406, USA. knowelj@stanford.edu
Themistocles L Assimes
Jun Li
Thomas Quertermous
John P Cooke
Stanford University · US

Funding

XOLAIR IN SUBJECTS WITH MODERATE TO SEVERE ATOPIC DERMATITIS WITH FOOD ALLERGYM01RR000070 · NCRR · STANFORD UNIVERSITY · PI RASGON, NATALIE L · 1985 to 2008
$32.4M
Genetic Determinants of PADR01HL075774 · NHLBI · STANFORD UNIVERSITY · PI COOKE, JOHN P · 2003 to 2007
$5.0M
Phase 2: NOs pathway in arterial diseaseR01HL063685 · NHLBI · STANFORD UNIVERSITY · PI COOKE, JOHN P · 2000 to 2004
$2.2M
VASCULAR BIOLOGY AND MEDICINE TRAININGT32HL007708 · NHLBI · STANFORD UNIVERSITY · PI COOKE, JOHN P · 1992 to 2007
$1.9M
NCRR NIH HHS M01 RR000070NCRR NIH HHS M01 RR 00070NHLBI NIH HHS R01 HL063685NHLBI NIH HHS R01 HL075774NHLBI NIH HHS R01 HL63685NHLBI NIH HHS T32 HL007708NHLBI NIH HHS T32 HL07708
6 · The paper itself

Abstract

Peripheral arterial disease (PAD) is characterized by reduced blood flow to the limbs, usually as a consequence of atherosclerosis, and affects approximately 12 million Americans. It is a common cause of cardiovascular morbidity and an independent predictor of cardiovascular mortality. Similar to other atherosclerotic diseases, such as coronary artery disease, PAD is the result of the complex interplay between injurious environmental stimuli and genetic predisposing factors of the host. Genetic susceptibility to PAD is likely contributed by sequence variants in multiple genes, each with modest effects. Although many of these variants probably alter susceptibility both to PAD and to coronary artery disease, it is likely that there exists a set of variants specifically to alter susceptibility to PAD. Despite the prevalence of PAD and its high societal burden, relatively little is known about such genetic variants. This review summarizes our limited present knowledge and gives an overview of recent, more powerful approaches to elucidating the genetic basis of PAD. We discuss the advantages and limitations of genetic studies and highlight the need for collaborative networks of PAD investigators for shedding light on this dark corner of vascular biology.

Indexed as

Genetic LinkageBiasCase-Control StudiesCooperative BehaviorData Interpretation, StatisticalGenetic Predisposition to DiseaseGenotypeHumansLinkage DisequilibriumMicrosatellite RepeatsPedigreePeripheral Vascular DiseasesPhenotypePolymorphism, Single NucleotideResearch DesignRisk Assessment

Identifiers

PMID17656669
PMCPMC4321902
OpenAlexW2075821102

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.