Evidence map›Paper›PMID 18204052›Full record

ArticleHuman molecular genetics2008

Comprehensive genetic analysis of the platelet activating factor acetylhydrolase (PLA2G7) gene and cardiovascular disease in case-control and family datasets.

Beth S Sutton, David R Crosslin, Svati H Shah, Sarah C Nelson, Anthony Bassil, A Brent Hale, Carol Haynes, Pascal J Goldschmidt-Clermont, Jeffery M Vance, David Seo and 3 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Human molecular genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 5 pooled it
2.5field-weighted citation impact, top 11% 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

49 citing papers in PubMed, 5 syntheses or guidelines pooled it, 72 citations in OpenAlex.

  1. Pooled it
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  8. Article
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  10. Sex-dimorphic gene effects on survival outcomes in people with coronary artery disease.American heart journal plus : cardiology research and practice · 2022
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  11. Review
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  20. The rs1051931 G>A Polymorphism in theFrontiers in pediatrics · 2020
    Article
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

13 authors at 6 institutions in 2 countries.

Beth S SuttonCenter for Human Genetics, Duke University Medical Center, Durham, NC 27710, USA.
David R Crosslin
Svati H Shah
Sarah C Nelson
Anthony Bassil
A Brent Hale
Carol Haynes
Pascal J Goldschmidt-Clermont
Jeffery M Vance
David Seo
William E Kraus
Simon G Gregory
Elizabeth R Hauser
Center for Human Genetics · USDuke Medical Center · USDuke University Hospital · USMiller College · USMiller Group (Canada) · CAUniversity of Miami · US

Funding

SNP discoveryP01HL073042 · NHLBI · DUKE UNIVERSITY · PI NEVINS, JOSEPH R · 2002 to 2006
$13.5M
GENECARD-Gene Identification in Early-Onset CADR01HL073389 · NHLBI · DUKE UNIVERSITY · PI HAUSER, ELIZABETH R · 2003 to 2007
$3.5M
NHLBI NIH HHS HL073389NHLBI NIH HHS HL73042-04NHLBI NIH HHS P01 HL073042NHLBI NIH HHS R01 HL073389
6 · The paper itself

Abstract

Platelet-activating factor acetylhydrolase (PLA2G7) is a potent pro- and anti-inflammatory molecule that has been implicated in multiple inflammatory disease processes, including cardiovascular disease. The goal of this study was to investigate the genetic effects of PLA2G7 on coronary artery disease (CAD) risk in two large, independent datasets with CAD. Using a haplotype tagging (ht) approach, 19 ht single nucleotide polymorphisms (SNPs) were genotyped in CATHGEN case-control samples (cases = 806 and controls = 267) and in the GENECARD Family Study (n = 1101 families, 2954 individuals). Single SNP analysis using logistic regression revealed nine SNPs with significant association in all CATHGEN subjects (P = 0.0004-0.02). CATHGEN cases were further stratified into subgroups based on age of CAD onset (AOO) and severity of disease; 599 young affecteds (YA, AOO <56) and 207 old affected (OA, AOO >56). Significant genetic effects were observed in both OA and YA (P = 0.0001-0.02). The GENECARD probands demonstrated results similar to those seen in the YA CATHGEN cases (P = 0.002-0.05). Of the 19 SNPs genotyped, 3 SNPs result in nonsynonymous coding changes (I198T, A379V and R92H). Two of the coding SNPs, R92H and A379V, constitute two of the most significantly associated SNPs, even after Bonferroni correction and appear to represent independent associations (r(2) = 0.09). Multiple additional polymorphisms in low linkage disequilibrium with these coding SNPs were also strongly associated. In summary, PLA2G7 represents an important, potentially functional candidate in the pathophysiology of CAD based on replicated associations using two independent datasets and multiple statistical approaches. Further functional studies involving a combination of risk alleles are warranted.

Indexed as

Polymorphism, Single Nucleotide1-Alkyl-2-acetylglycerophosphocholine EsteraseAdultAgedAge of OnsetAortaCase-Control StudiesCoronary Artery DiseaseFamilyFemaleHaplotypesHumansLinkage DisequilibriumMaleMiddle AgedNorth Carolina1-Alkyl-2-acetylglycerophosphocholine EsterasePhospholipases A2PLA2G7 protein, human

Identifiers

PMID18204052
PMCPMC2652668
OpenAlexW2119217476

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.