Department of Physiology, Fasa University of Medical Sciences, Fasa, Iran.
J Renin Angiotensin Aldosterone Syst. 2021 Nov 8;2021:6824259. doi: 10.1155/2021/6824259. eCollection 2021.
Coronavirus disease 2019 (COVID-19) can occur due to contracting severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 has no confined treatment and, consequently, has high hospitalization and mortality rates. Moreover, people who contract COVID-19 present systemic inflammatory spillover. It is now known that COVID-19 pathogenesis is linked to the renin-angiotensin system (RAS). COVID-19 invades host cells via the angiotensin-converting enzyme 2 (ACE2) receptor-as such, an individual's susceptibility to COVID-19 increases alongside the upregulation of this receptor. COVID-19 has also been associated with interstitial pulmonary fibrosis, which leads to acute respiratory distress, cardiomyopathy, and shock. These outcomes are thought to result from imbalances in angiotensin (Ang) II and Ang-(1-7)/alamandine activity. ACE2, Ang-(1-7), and alamandine have potent anti-inflammatory properties, and some SARS-CoV-2 patients exhibit high levels of ACE2 and Ang-(1-7). This phenomenon could indicate a failing physiological response to prevent or reduce the severity of inflammation-mediated pulmonary injuries. Alamandine, which is another protective component of the RAS, has several health benefits owing to its antithrombogenic, anti-inflammatory, and antifibrotic characteristics. Alamandine alleviates pulmonary fibrosis via the Mas-related G protein-coupled receptor D (MrgD). Thus, a better understanding of this pathway could uncover novel pharmacological strategies for altering proinflammatory environments within the body. Following such strategies could inhibit fibrosis after SARS-CoV-2 infection and, consequently, prevent COVID-19.
新型冠状病毒病（COVID-19）是由严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）引起的。COVID-19 目前没有明确的治疗方法，因此具有较高的住院率和死亡率。此外，感染 COVID-19 的患者会出现全身性炎症溢出。现在已知 COVID-19 的发病机制与肾素-血管紧张素系统（RAS）有关。COVID-19 通过血管紧张素转换酶 2（ACE2）受体进入宿主细胞，因此，个体对 COVID-19 的易感性随着该受体的上调而增加。COVID-19 还与间质性肺纤维化有关，导致急性呼吸窘迫、心肌病和休克。这些结果被认为是血管紧张素（Ang）II 和 Ang-(1-7)/alamandine 活性失衡的结果。ACE2、Ang-(1-7) 和 alamandine 具有强大的抗炎特性，一些 COVID-19 患者表现出高水平的 ACE2 和 Ang-(1-7)。这种现象可能表明生理反应失败，无法预防或减轻炎症介导的肺损伤的严重程度。alamandine 是 RAS 的另一个保护成分，由于其抗血栓形成、抗炎和抗纤维化特性，具有多种健康益处。alamandine 通过 MrgD 减轻肺纤维化。因此，更好地了解这一途径可以揭示改变体内促炎环境的新的药理学策略。遵循这些策略可以抑制 SARS-CoV-2 感染后的纤维化，从而预防 COVID-19。
