Common variation in atrial fibrillation: navigating the path from genetic association to mechanism.

Cardiovasc Res
Authors
Keywords
Abstract

Atrial fibrillation (AF) is the most common cardiac arrhythmia with well-established clinical and genetic risk components. Genome-wide association studies (GWAS) have identified 17 independent susceptibility signals for AF at 14 genomic regions, but the mechanisms through which these loci confer risk to AF remain largely undefined. This problem is not unique to AF, as the field of functional genomics, which attempts to bridge this gap from genotype to phenotype, has only uncovered the mechanisms for a handful of GWAS loci. Recent functional genomic studies have made great strides towards translating genetic discoveries to an underlying mechanism, but the large-scale application of these techniques to AF has remain limited. These advances, as well as the continued unresolved challenges for both common variation in AF and the functional genomics field in general, will be the subject of the following review.

Year of Publication
2016
Journal
Cardiovasc Res
Volume
109
Issue
4
Pages
493-501
Date Published
2016 Apr 01
ISSN
1755-3245
URL
DOI
10.1093/cvr/cvv283
PubMed ID
26733238
PubMed Central ID
PMC4777911
Links
Grant list
R01HL128914 / HL / NHLBI NIH HHS / United States
R01 HL092577 / HL / NHLBI NIH HHS / United States
K24HL105780 / HL / NHLBI NIH HHS / United States
T32 HL007208 / HL / NHLBI NIH HHS / United States
1R01HL092577 / HL / NHLBI NIH HHS / United States