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. 2021 Dec 2:cvab342. doi: 10.1093/cvr/cvab342

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This article has been co-published with permission in the European Heart Journal and Cardiovascular Research. © The European Society of Cardiology 2021. All rights reserved. The articles are identical except for minor stylistic and spelling differences in keeping with each journal's style. Either citation can be used when citing this article.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

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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Critical role of ACE2 in the regulation of SARS-CoV-2 infection in ACE2-expressing cells^a (A) and ACE2 reduced surface expression by ADAMTS17 (B). (A) SARS-CoV-2 spike protein (S1) is primed by the serine protease transmembrane protein serine 2, which enables its interaction with the membrane bound form of ACE2. This is required for virus internalization and subsequent replication. Other receptors can also facilitate the entry of SARS-CoV-2, e.g. neuropilin 1. (B) Membrane bound ACE2 may be shed from the cell membrane by ADAMTS17 producing soluble ACE2. This mechanism may limit viral invasion. ACE2, ACE2; ADAMTS17, a disintegrin and metalloproteinase with thrombospondin motifs 17; NRP1, neuropilin-1; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; S1, spike protein 1; TMPRSS2, transmembrane protease serine 2. ^aThis includes type 2 pneumocytes, cardiomyocytes, pericytes, endothelium, and possibly other cell types.