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Yao, C.* ; Chen, G.* ; Song, C.* ; Keefe, J.* ; Mendelson, M.* ; Huan, T.* ; Sun, B.B.* ; Laser, A. ; Maranville, J.C.* ; Wu, H.* ; Ho, J.E.* ; Courchesne, P.* ; Lyass, A.* ; Larson, M.G.* ; Gieger, C. ; Graumann, J.* ; Johnson, A.D.* ; Danesh, J.* ; Runz, H.* ; Hwang, S.-J.* ; Liu, C.* ; Butterworth, A.S.* ; Suhre, K.* ; Levy, D.*

Genome-wide mapping of plasma protein QTLs identifies putatively causal genes and pathways for cardiovascular disease.

Nat. Commun. 9:3268 (2018)
Publ. Version/Full Text DOI PMC
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Identifying genetic variants associated with circulating protein concentrations (protein quantitative trait loci; pQTLs) and integrating them with variants from genome-wide association studies (GWAS) may illuminate the proteome’s causal role in disease and bridge a knowledge gap regarding SNP-disease associations. We provide the results of GWAS of 71 high-value cardiovascular disease proteins in 6861 Framingham Heart Study participants and independent external replication. We report the mapping of over 16,000 pQTL variants and their functional relevance. We provide an integrated plasma protein-QTL database. Thirteen proteins harbor pQTL variants that match coronary disease-risk variants from GWAS or test causal for coronary disease by Mendelian randomization. Eight of these proteins predict new-onset cardiovascular disease events in Framingham participants. We demonstrate that identifying pQTLs, integrating them with GWAS results, employing Mendelian randomization, and prospectively testing protein-trait associations holds potential for elucidating causal genes, proteins, and pathways for cardiovascular disease and may identify targets for its prevention and treatment.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Coronary-artery-disease; Abo Blood-group; Heart-disease; Association; Variants; Expression; Atherosclerosis; Metaanalysis; Framingham; Risk
Language english
Publication Year 2018
HGF-reported in Year 2018
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Journal Nature Communications
Quellenangaben Volume: 9, Issue: 1, Pages: , Article Number: 3268 Supplement: ,
Publisher Nature Publishing Group
Publishing Place London
Reviewing status Peer reviewed
Institute(s) Institute of Epidemiology (EPI)
POF-Topic(s) 30202 - Environmental Health
Research field(s) Genetics and Epidemiology
PSP Element(s) G-504091-004
DOI 10.1038/s41467-018-05512-x
WOS ID WOS:000441608900008
Scopus ID 85051677773
PubMed ID 30111768
Erfassungsdatum 2018-09-14
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