Laboratório de Biologia Celular e Tecidual, Programa de Pós-Graduação em Biologia Celular e Molecular, Escola de Ciências da Saúde e da Vida, Pontifícia Universidade Católica do Rio Grande do Sul, PUCRS, Porto Alegre, Brazil.
Programa de Pós-Graduação em Biotecnologia (PPGBiotec), Programa de Pós-Graduação em Ciências Médicas (PPGCM), Universidade do Vale do Taquari-UNIVATES, Lajeado, Brazil.
Front Immunol. 2021 Jan 14;11:577875. doi: 10.3389/fimmu.2020.577875. eCollection 2020.
Human infection by the SARS-CoV-2 is causing the current COVID-19 pandemic. With the growing numbers of cases and deaths, there is an urgent need to explore pathophysiological hypotheses in an attempt to better understand the factors determining the course of the disease. Here, we hypothesize that COVID-19 severity and its symptoms could be related to transmembrane and soluble Angiotensin-converting enzyme 2 (tACE2 and sACE2); Angiotensin II (ANG II); Angiotensin 1-7 (ANG 1-7) and angiotensin receptor 1 (AT1R) activation levels. Additionally, we hypothesize that an early peak in ANG II and ADAM-17 might represent a physiological attempt to reduce viral infection tACE2. This viewpoint presents: (1) a brief introduction regarding the renin-angiotensin-aldosterone system (RAAS), detailing its receptors, molecular synthesis, and degradation routes; (2) a description of the proposed early changes in the RAAS in response to SARS-CoV-2 infection, including biological scenarios for the best and worst prognoses; and (3) the physiological pathways and reasoning for changes in the RAAS following SARS-CoV-2 infection.
人类感染 SARS-CoV-2 是导致当前 COVID-19 大流行的原因。随着病例和死亡人数的不断增加，迫切需要探索病理生理学假说，试图更好地了解决定疾病进程的因素。在这里，我们假设 COVID-19 的严重程度及其症状可能与跨膜和可溶性血管紧张素转换酶 2（tACE2 和 sACE2）；血管紧张素 II（ANG II）；血管紧张素 1-7（ANG 1-7）和血管紧张素受体 1（AT1R）的激活水平有关。此外，我们假设 ANG II 和 ADAM-17 的早期峰值可能代表一种降低病毒感染 tACE2 的生理尝试。这一观点提出：（1）简要介绍肾素-血管紧张素-醛固酮系统（RAAS），详细说明其受体、分子合成和降解途径；（2）描述 SARS-CoV-2 感染后 RAAS 的早期变化，包括最佳和最差预后的生物学情景；（3）SARS-CoV-2 感染后 RAAS 变化的生理途径和推理。
