Back

Discovery and systematic characterization of risk variants and genes for coronary artery disease in over a million participants.

Aragam, K. G.; Jiang, T.; Goel, A.; Kanoni, S.; Wolford, B. N.; Weeks, E. M.; Wang, M.; Hindy, G.; Zhou, W.; Grace, C.; Roselli, C.; Marston, N. A.; Kamanu, F. K.; Surakka, I.; Munoz Venegas, L.; Sherliker, P.; Koyama, S.; Ishigaki, K.; Asvold, B. O.; Brown, M. R.; Brumpton, B.; de Vries, P. S.; Giannakopoulou, O.; Giardoglou, P.; Gudbjartsson, D. F.; Guldener, U.; Haider, S. M. I.; Helgadottir, A.; Ibrahim, M.; Kastrati, A.; Kessler, T.; Li, L.; Ma, L.; Meitinger, T.; Mucha, S.; Munz, M.; Murgia, F.; Nielsen, J. B.; Nothen, M. M.; Pang, S.; Reinberger, T.; Thorleifsson, G.; von Scheidt, M.; U

2021-06-02 genetic and genomic medicine
10.1101/2021.05.24.21257377 medRxiv
Show abstract

Rapid progress of the discovery of genetic loci associated with common, complex diseases has outpaced the elucidation of mechanisms pertinent to disease pathogenesis. To address relevant barriers for coronary artery disease (CAD), we combined genetic discovery analyses with downstream characterization of likely causal variants, genes, and biological pathways. Specifically, we conducted a genome-wide association study (GWAS) comprising 181,522 cases of CAD among 1,165,690 participants. We detected 241 associations, including 54 associations and 30 loci not previously linked to CAD. Next, we prioritized likely causal variants using functionally-informed fine-mapping, yielding 42 associations with fewer than five variants in the 95% credible set. Combining eight complementary predictors, we prioritized 185 candidate causal genes, including 94 genes supported by three or more predictors. Similarity-based clustering underscored a role for early developmental processes, cell cycle signaling, and vascular proliferation in the pathogenesis of CAD. Our analysis identifies and systematically characterizes risk loci for CAD to inform experimental interrogation of putative causal mechanisms for CAD.

Matching journals

The top 5 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.