肾素-血管紧张素系统在COVID-19发病机制中的作用及可能的药物靶点

S. Shankar, Arvind Kumar, Diksha Patidar, Sai Kanukuntla, N. Wig
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引用次数: 0

摘要

2019冠状病毒病(COVID-19)的特征是发烧、咳嗽、呼吸短促、肌痛和头痛。该病也有更严重的形式,表现为危及生命的急性呼吸窘迫综合征、急性心脏损伤、急性肾损伤、弥散性血管内凝血病和细胞因子风暴。已经阐明,与其前身SARS冠状病毒一样,SARS冠状病毒-2利用血管紧张素转换酶2受体进入细胞。这一知识引发了对肾素-血管紧张素系统(RAS)失调在COVID-19发病机制中的作用的猜测。有人提出,RAS失调的影响会导致炎症级联反应,并导致细胞因子风暴,这是该疾病的核心。本文从RAS通路出发,推测RAS正反馈回路在新冠肺炎发病机制中的可能性。
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Renin-angiotensin system in the pathogenesis of COVID-19 and possible drug targets
Coronavirus disease 2019 (COVID-19) is characterized by fever, cough, shortness of breath, myalgia, and headache. The disease also takes a more severe form with life-threatening manifestations of acute respiratory distress syndrome, acute cardiac injury, acute kidney injury, disseminated intravascular coagulopathy, and cytokine storm. It has been elucidated that like its predecessor, the SARS CoV, the SARS CoV-2 utilizes the angiotensin-converting enzyme 2 receptor to enter cells. This knowledge brought into speculation the effects of a dysregulated renin-angiotensin system (RAS) in the pathogenesis of COVID-19. It has been proposed that the effects of a dysregulated RAS would lead to an inflammatory cascade and contribute to the cytokine storm that is central to the disease. This paper looks at the RAS pathway and hypothesizes the possibility of a positive RAS feedback loop in the pathogenesis of COVID-19.
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