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. 2021 Aug 29;10(17):3885. doi: 10.3390/jcm10173885

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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The counter-regulatory renin–angiotensin system (RAS) axis in the lungs in the coronavirus disease 2019 (COVID-19) setting. Angiotensin-converting enzyme 2 (ACE2) serves as the severe acute respiratory syndrome coronavirus (SARS-CoV)-2 receptor, whereas the proinflammatory prolyloligopeptidase (POP) converts less effectively than ACE2 the deleterious angiotensin (ANG) II to the protective ANG (1–7). As a result, deleterious signalling (inflammation, thrombosis and fibrosis) dominates over protective (vasodilation, vasoprotection and tissue protection) signalling in patients with severe COVID-19, which may lead to acute lung injury. Abbreviations: AT1R, angiotensin receptor type 1; AT2R, angiotensin receptor type 2 [45].