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. 2022 May 26;9:901245. doi: 10.3389/fcvm.2022.901245

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Copyright © 2022 Izquierdo-Marquisá, Cubero-Gallego, Aparisi, Vaquerizo and Ribas-Barquet.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Pathophysiology of COVID-19 [adapted from Gupta et al. (18)]: (1) Direct virus-mediated cell damage. SARS-CoV-2 enters into host cells through the union between the spike protein and ACE2 receptor in the presence of TMPRSS2 protease; (2) Downregulation of ACE2 leads to a dysregulation of the RAAS and consequently to an increase of angiotensin I and angiotensin II; (3) Virus entrance to endothelial cell damage induces apoptosis and endothelialitis; (4) T-cell lymphopenia, inhibition of interferon signaling and hyperactive innate immunity produces a dysregulation of the immune response and a cytokine storm syndrome.