Evidence map›Paper›PMID 28355232›Full record

ArticlePloS one2017

A genome-wide trans-ethnic interaction study links the PIGR-FCAMR locus to coronary atherosclerosis via interactions between genetic variants and residential exposure to traffic.

Cavin K Ward-Caviness, Lucas M Neas, Colette Blach, Carol S Haynes, Karen LaRocque-Abramson, Elizabeth Grass, Z Elaine Dowdy, Robert B Devlin, David Diaz-Sanchez, Wayne E Cascio and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Gene-Environment Interactions for Cardiovascular Disease.Current atherosclerosis reports · 2021
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  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

15 authors at 3 institutions in 2 countries.

Cavin K Ward-CavinessDuke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, United States of America.ORCID http://orcid.org/0000-0002-6322-4349
Lucas M NeasNational Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Chapel Hill, NC, United States of America.
Colette BlachDuke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, United States of America.
Carol S HaynesDuke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, United States of America.
Karen LaRocque-AbramsonDuke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, United States of America.
Elizabeth GrassDuke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, United States of America.
Z Elaine DowdyDuke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, United States of America.
Robert B DevlinNational Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Chapel Hill, NC, United States of America.
David Diaz-SanchezNational Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Chapel Hill, NC, United States of America.
Wayne E CascioNational Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Chapel Hill, NC, United States of America.
Marie Lynn MirandaNational Center for Geospatial Medicine, Rice University, Houston, TX, United States of America.
Simon G GregoryDuke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, United States of America.
Svati H ShahDuke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, United States of America.
William E KrausDuke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, United States of America.
Elizabeth R HauserDuke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, United States of America.
Duke University · USEnvironmental Protection Agency · USRice University · US

Funding

The Genetics Of Biobehavioral Risk Factors For CVDP01HL036587 · NHLBI · DUKE UNIVERSITY · PI KRAUS, WILLIAM E · 1986 to 2020
$35.9M
Metabolomic Quantitative Trait Locus (mQTL) Genetic Mapping in Human CVDR01HL095987 · NHLBI · DUKE UNIVERSITY · PI SHAH, SVATI H. · 2009 to 2013
$3.4M
NHLBI NIH HHS P01 HL036587NHLBI NIH HHS R01 HL095987
6 · The paper itself

Abstract

Air pollution is a worldwide contributor to cardiovascular disease mortality and morbidity. Traffic-related air pollution is a widespread environmental exposure and is associated with multiple cardiovascular outcomes such as coronary atherosclerosis, peripheral arterial disease, and myocardial infarction. Despite the recognition of the importance of both genetic and environmental exposures to the pathogenesis of cardiovascular disease, studies of how these two contributors operate jointly are rare. We performed a genome-wide interaction study (GWIS) to examine gene-traffic exposure interactions associated with coronary atherosclerosis. Using race-stratified cohorts of 538 African-Americans (AA) and 1562 European-Americans (EA) from a cardiac catheterization cohort (CATHGEN), we identify gene-by-traffic exposure interactions associated with the number of significantly diseased coronary vessels as a measure of chronic atherosclerosis. We found five suggestive (P<1x10-5) interactions in the AA GWIS, of which two (rs1856746 and rs2791713) replicated in the EA cohort (P < 0.05). Both SNPs are in the PIGR-FCAMR locus and are eQTLs in lymphocytes. The protein products of both PIGR and FCAMR are implicated in inflammatory processes. In the EA GWIS, there were three suggestive interactions; none of these replicated in the AA GWIS. All three were intergenic; the most significant interaction was in a regulatory region associated with SAMSN1, a gene previously associated with atherosclerosis and B cell activation. In conclusion, we have uncovered several novel genes associated with coronary atherosclerosis in individuals chronically exposed to increased ambient concentrations of traffic air pollution. These genes point towards inflammatory pathways that may modify the effects of air pollution on cardiovascular disease risk.

Indexed as

Genetic LociQuantitative Trait LociAdaptor Proteins, Vesicular TransportAgedAir PollutionAtherosclerosisBlack or African AmericanCardiac CatheterizationCoronary Artery DiseaseEnvironmental ExposureFemaleGene-Environment InteractionGenome, HumanGenome-Wide Association StudyHumansLymphocyte ActivationAdaptor Proteins, Vesicular TransportFcalpha-mu receptor, humanMembrane ProteinsOSCAR protein, humanReceptors, Cell SurfaceReceptors, FcSAMSN1 protein, humanVehicle Emissions

Identifiers

PMID28355232
PMCPMC5371323
OpenAlexW2600054484

What OpenQuestion holds

Textmetadata
LicenceCC0
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.