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Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Abstract:
Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/s41467-019-13690-5

Authors


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Role:
Author
ORCID:
0000-0001-7422-2288
More by this author
Role:
Author
ORCID:
0000-0001-5267-6756
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Role:
Author
ORCID:
0000-0003-3043-3942


Publisher:
Springer Nature
Journal:
Nature Communications More from this journal
Volume:
11
Issue:
1
Article number:
163
Publication date:
2020-01-09
Acceptance date:
2019-11-18
DOI:
EISSN:
2041-1723
ISSN:
2041-1723
Pmid:
31919418


Language:
English
Keywords:
Pubs id:
1081909
Local pid:
pubs:1081909
Deposit date:
2020-04-06

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