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. 2022 Apr 7;145(18):1398–1411. doi: 10.1161/CIRCULATIONAHA.121.057888

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© 2022 The Authors.

Circulation is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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Figure 4. — Causal inference between plasma ACE2 and COVID-19 based on the ACE2 cis-pQTL. A, The regional genome-wide association study z scores across 4 traits are compared; alleles are coded so that the estimated single nucleotide polymorphism (SNP) effects on ACE2 (angiotensin-converting enzyme 2) are all positive. Genome-wide significant SNPs for ACE2 (P<5×10⁻⁸) are highlighted in yellow. The 3 SNPs representing independent significant associations after linkage disequilibrium (LD) clumping (r²<0.001) are marked in red. B, Inference of the causal effect of ACE2 on COVID-19 through mendelian randomization (MR). The MR was performed with an inverse-variance weighted causal effect estimator based on multiple genome-wide significant cis-regulatory SNPs. A threshold of R²<0.001 was applied to prune out SNPs in LD. Whiskers represent 95% CIs. OR indicates odds ratio.