RAAS, ACE2 and COVID-19; a mechanistic review.

RAAS,ACE2 和 COVID - 19 ； 机理综述。

• 影响指数: 4.052
• 发表时间: Nov 2021
• 来源期刊: Saudi J Biol Sci
• DOI: 10.1016/j.sjbs.2021.07.003
• PMID: 34305426
• 文章类型: Journal Article
• 作者列表: Elshafei A,Khidr EG,El-Husseiny AA,Gomaa MH

关键词: ACE1, angiotensin-converting enzyme 1; ACE2; ACE2, angiotensin-converting enzyme 2; ACEIs; ACEIs, angiotensin-converting enzyme inhibitors; AEC-II, alveolar epithelial type II cells; ARBs; ARBs, angiotensin receptor blockers; AT1R, angiotensin type 1 receptor; AT2R, angiotensin type 2 receptor; Ang 1-7, angiotensin 1-7; Ang 1-9, angiotensin 1-9; AngI, angiotensin I; AngII, angiotensin II; Angiotensin 1–7; Angiotensin II; COVID-19; COVID-19, coronavirus disease 2019; CVD, cardiovascular disease; ERK, extracellular signal-regulated kinase; ICU, intensive care unit; MAPK, mitogen-activated protein kinase; NLRP3, (NOD, LRR, and pyrin domain-containing protein 3); RAAS, renin-angiotensin-aldosterone system; TGF-β, transforming growth factor-beta; miR-21, microRNA-21

Abstract

The use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) in coronavirus disease 2019 (COVID-19) patients has been claimed as associated with the risk of COVID-19 infection and its subsequent morbidities and mortalities. These claims were resulting from the possibility of upregulating the expression of angiotensin-converting enzyme 2 (ACE2), facilitation of SARS-CoV-2 entry, and increasing the susceptibility of infection in such treated cardiovascular patients. ACE2 and renin-angiotensin-aldosterone system (RAAS) products have a critical function in controlling the severity of lung injury, fibrosis, and failure following the initiation of the disease. This review is to clarify the mechanisms beyond the possible deleterious effects of angiotensin II (Ang II), and the potential protective role of angiotensin 1-7 (Ang 1-7) against pulmonary fibrosis, with a subsequent discussion of the latest updates on ACEIs/ARBs use and COVID-19 susceptibility in the light of these mechanisms and biochemical explanation.

摘要

在2019年冠状病毒病（COVID-19）患者中使用血管紧张素转换酶抑制剂（ACEI）和血管紧张素受体阻滞剂（ARB）被认为与COVID-19感染的风险及其随后的发病率和死亡率有关。这些说法是由于上调血管紧张素转换酶2（ACE2）表达的可能性，促进SARS-CoV-2进入，并增加此类治疗的心血管患者的感染易感性。ACE2和肾素-血管紧张素-醛固酮系统（RAAS）产品在控制肺损伤的严重程度方面具有关键功能，纤维化，和疾病开始后的失败。这篇综述旨在阐明血管紧张素II（AngII）可能有害作用之外的机制。以及血管紧张素1-7（Ang1-7）对肺纤维化的潜在保护作用，随后根据这些机制和生化解释讨论了ACEI/ARBs使用和COVID-19易感性的最新更新。