Shared genetic risk factors and causal association between psoriasis and coronary artery disease

Matthew T. Patrick, Qinmengge Li, Rachael Wasikowski, Nehal Mehta, Johann E. Gudjonsson, James T. Elder, Xiang Zhou and Lam C. Tsoi ()
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Matthew T. Patrick: University of Michigan
Qinmengge Li: University of Michigan
Rachael Wasikowski: University of Michigan
Nehal Mehta: National Institutes of Health
Johann E. Gudjonsson: University of Michigan
James T. Elder: University of Michigan
Xiang Zhou: University of Michigan
Lam C. Tsoi: University of Michigan

Nature Communications, 2022, vol. 13, issue 1, 1-12

Abstract: Abstract Psoriasis and coronary artery disease (CAD) are related comorbidities that are well established, but whether a genetic basis underlies this is not well studied. We apply trans-disease meta-analysis to 11,024 psoriasis and 60,801 CAD cases, along with their associated controls, identifying one opposing and three shared genetic loci, which are confirmed through colocalization analysis. Combining results from Bayesian credible interval analysis with independent information from genomic, epigenomic, and spatial chromatin organization, we prioritize genes (including IFIH1 and IL23A) that have implications for common molecular mechanisms involved in psoriasis and CAD inflammatory signaling. Chronic systemic inflammation has been associated with CAD and myocardial infarction, and Mendelian randomization analysis finds that CAD as an exposure can have a significant causal effect on psoriasis (OR = 1.11; p = 3×10−6) following adjustment for BMI and waist-hip ratio. Together, these findings suggest that systemic inflammation which causes CAD can increase the risk of psoriasis.

Date: 2022
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-34323-4

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DOI: 10.1038/s41467-022-34323-4

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