Faculty of Sciences 2, Department of Biology, Lebanese University, Campus Fanar, Jdeidet El-Matn, Beirut P.O. Box 90656, Lebanon.
Faculty of Sciences 3, Department of Biology, Lebanese University, Campus Michel Slayman Ras Maska, Tripoli 1352, Lebanon.
Molecules. 2022 Mar 22;27(7):2048. doi: 10.3390/molecules27072048.
The binding of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike glycoprotein to its cellular receptor, the angiotensin-converting enzyme 2 (ACE2), causes its downregulation, which subsequently leads to the dysregulation of the renin-angiotensin system (RAS) in favor of the ACE-angiotensin II (Ang II)-angiotensin II type I receptor (AT1R) axis. AT1R has a major role in RAS by being involved in several physiological events including blood pressure control and electrolyte balance. Following SARS-CoV-2 infection, pathogenic episodes generated by the vasoconstriction, proinflammatory, profibrotic, and prooxidative consequences of the Ang II-AT1R axis activation are accompanied by a hyperinflammatory state (cytokine storm) and an acute respiratory distress syndrome (ARDS). AT1R, a member of the G protein-coupled receptor (GPCR) family, modulates Ang II deleterious effects through the activation of multiple downstream signaling pathways, among which are MAP kinases (ERK 1/2, JNK, p38MAPK), receptor tyrosine kinases (PDGF, EGFR, insulin receptor), and nonreceptor tyrosine kinases (Src, JAK/STAT, focal adhesion kinase (FAK)), and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. COVID-19 is well known for generating respiratory symptoms, but because ACE2 is expressed in various body tissues, several extrapulmonary pathologies are also manifested, including neurologic disorders, vasculature and myocardial complications, kidney injury, gastrointestinal symptoms, hepatic injury, hyperglycemia, and dermatologic complications. Therefore, the development of drugs based on RAS blockers, such as angiotensin II receptor blockers (ARBs), that inhibit the damaging axis of the RAS cascade may become one of the most promising approaches for the treatment of COVID-19 in the near future. We herein review the general features of AT1R, with a special focus on the receptor-mediated activation of the different downstream signaling pathways leading to specific cellular responses. In addition, we provide the latest insights into the roles of AT1R in COVID-19 outcomes in different systems of the human body, as well as the role of ARBs as tentative pharmacological agents to treat COVID-19.
严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)刺突糖蛋白与细胞受体血管紧张素转换酶 2(ACE2)的结合导致其下调,进而导致肾素-血管紧张素系统(RAS)失稳,有利于 ACE-血管紧张素 II(Ang II)-血管紧张素 II 型受体(AT1R)轴。AT1R 通过参与包括血压控制和电解质平衡在内的几种生理事件,在 RAS 中起主要作用。在 SARS-CoV-2 感染后,Ang II-AT1R 轴激活产生的血管收缩、促炎、纤维化和促氧化等致病作用,伴随着过度炎症状态(细胞因子风暴)和急性呼吸窘迫综合征(ARDS)。AT1R 是 G 蛋白偶联受体(GPCR)家族的成员,通过激活多种下游信号通路来调节 Ang II 的有害作用,其中包括丝裂原活化蛋白激酶(ERK 1/2、JNK、p38MAPK)、受体酪氨酸激酶(血小板衍生生长因子、表皮生长因子受体、胰岛素受体)和非受体酪氨酸激酶(Src、JAK/STAT、黏着斑激酶(FAK))和烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶。COVID-19 以产生呼吸道症状而闻名,但由于 ACE2 在各种身体组织中表达,也表现出多种肺外病理学,包括神经紊乱、血管和心肌并发症、肾损伤、胃肠道症状、肝损伤、高血糖和皮肤并发症。因此,基于 RAS 阻滞剂(如血管紧张素 II 受体阻滞剂(ARB))的药物的开发可能成为治疗 COVID-19 的最有前途的方法之一。本文综述了 AT1R 的一般特征,特别关注受体介导的不同下游信号通路的激活导致特定的细胞反应。此外,我们还提供了 AT1R 在人体不同系统 COVID-19 结局中的最新作用,以及 ARB 作为治疗 COVID-19 的暂定药理学药物的作用。