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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 3. — Genetic and causal relationships between plasma ACE2 and vascular diseases. Estimates significantly different from zero are highlighted in filled circles. First 2 forest plots show the bidirectional generalized summary-level mendelian randomization (GSMR) analysis results between plasma ACE2 (angiotensin-converting enzyme 2) and 48 vascular disease–related traits. Third forest plot gives the corresponding genetic correlations estimates between plasma ACE2 and these phenotypes. Last forest plot shows the estimated mendelian randomization (MR) effects based on cis–protein quantitative trait loci (pQTL) only. HDL indicates high-density lipoprotein; LDL, low-density lipoprotein; OR, odds ratio; and SAH, subarachnoid hemorrhage.