Evidence map›Paper›PMID 20442857›Full record

ArticlePLoS genetics2010

Genome-wide association study of Lp-PLA(2) activity and mass in the Framingham Heart Study.

Sunil Suchindran, David Rivedal, John R Guyton, Tom Milledge, Xiaoyi Gao, Ashlee Benjamin, Jennifer Rowell, Geoffrey S Ginsburg, Jeanette J McCarthy

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 5 pooled it
6.5field-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

39 citing papers in PubMed, 5 syntheses or guidelines pooled it, 75 citations in OpenAlex.

  1. Pooled it
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  6. Trial
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  8. Article
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  12. Article
  13. On the present and future role of Lp-PLAArchives of medical science : AMS · 2021
    Article
  14. Review
  15. A decade in psychiatric GWAS research.Molecular psychiatry · 2019
    Review
  16. Article
  17. Article
  18. The effects of PPARγ on the regulation of the TOMM40-APOE-C1 genes cluster.Biochimica et biophysica acta. Molecular basis of disease · 2017
    Article
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  20. 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

9 authors at 3 institutions in 1 country.

Sunil SuchindranInstitute for Genome Sciences and Policy, Duke University Medical Center, Durham, North Carolina, United States of America.
David Rivedal
John R Guyton
Tom Milledge
Xiaoyi Gao
Ashlee Benjamin
Jennifer Rowell
Geoffrey S Ginsburg
Jeanette J McCarthy
Duke Medical Center · USDuke University Hospital · USWashington University in St. Louis · US

Funding

Endocrinology and Metabolism Training ProgramT32DK007012 · NIDDK · DUKE UNIVERSITY · PI DAVID A. D'ALESSIO · 1986 to 2026
$6.8M
Computational Biology and Bioinformatics Training ProgramT32GM071340 · NIGMS · DUKE UNIVERSITY · PI MAGWENE, PAUL MITAARI · 2005 to 2020
$3.3M
Pharmacogenetics of lipid response to estrogen therapyR01HL085191 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI MCCARTHY, JEANETTE J · 2006 to 2009
$758k
NHLBI NIH HHS R01 HL085191NHLBI NIH HHS R01 HL085191-01NIDDK NIH HHS T32 DK007012NIGMS NIH HHS T32 GM071340
6 · The paper itself

Abstract

Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) is an emerging risk factor and therapeutic target for cardiovascular disease. The activity and mass of this enzyme are heritable traits, but major genetic determinants have not been explored in a systematic, genome-wide fashion. We carried out a genome-wide association study of Lp-PLA(2) activity and mass in 6,668 Caucasian subjects from the population-based Framingham Heart Study. Clinical data and genotypes from the Affymetrix 550K SNP array were obtained from the open-access Framingham SHARe project. Each polymorphism that passed quality control was tested for associations with Lp-PLA(2) activity and mass using linear mixed models implemented in the R statistical package, accounting for familial correlations, and controlling for age, sex, smoking, lipid-lowering-medication use, and cohort. For Lp-PLA(2) activity, polymorphisms at four independent loci reached genome-wide significance, including the APOE/APOC1 region on chromosome 19 (p = 6 x 10(-24)); CELSR2/PSRC1 on chromosome 1 (p = 3 x 10(-15)); SCARB1 on chromosome 12 (p = 1x10(-8)) and ZNF259/BUD13 in the APOA5/APOA1 gene region on chromosome 11 (p = 4 x 10(-8)). All of these remained significant after accounting for associations with LDL cholesterol, HDL cholesterol, or triglycerides. For Lp-PLA(2) mass, 12 SNPs achieved genome-wide significance, all clustering in a region on chromosome 6p12.3 near the PLA2G7 gene. Our analyses demonstrate that genetic polymorphisms may contribute to inter-individual variation in Lp-PLA(2) activity and mass.

Indexed as

Genetic Predisposition to Disease1-Alkyl-2-acetylglycerophosphocholine EsteraseCardiovascular DiseasesGenome, HumanGenome-Wide Association StudyGenotypeHumansPolymorphism, Single NucleotideRisk Factors1-Alkyl-2-acetylglycerophosphocholine Esterase

Identifiers

PMID20442857
PMCPMC2861686
OpenAlexW1990736759

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.