Department of Cardiac Surgery, Heart and Vascular Institute, Cleveland Clinic Abu Dhabi, Abu Dhabi, UAE.
Winramed Health Care Services Limited Company, Siófok, Hungary.
J Vasc Surg. 2021 Jun;73(6):1889-1897. doi: 10.1016/j.jvs.2020.12.056. Epub 2020 Dec 19.
Management of the pandemic caused by the novel coronavirus SARS-CoV-2 challenges both scientists and physicians to rapidly develop, and urgently assess, effective diagnostic tests and therapeutic interventions. The initial presentation of the disease in symptomatic patients is invariably respiratory, with dry cough being the main symptom, but an increasing number of reports reveal multiple-organ involvement. The aim of this review is to summarize the potential role of the renin-angiotensin system activated phagocytes in the pathogenesis of COVID-19 disease.
Data for this review were identified by searches of PubMed and references from relevant articles using the search terms "SARS," "COVID-19," "renin-angiotensin-system," "phagocyte," "reactive free radical," "antioxidant," "ARDS," "thrombosis," "myocardial," "ischaemia," "reperfusion," "microvascular," and "ACE2." Abstracts and reports from meetings were not included in this work. Only articles published in English between 1976 and 2020 were reviewed.
The cellular target of SARS viruses is the angiotensin-converting enzyme 2, a critical regulating protein in the renin-angiotensin system. The elimination of this enzyme by the viral spike protein results in excessive activation of phagocytes, migration into the tissues via the high endothelial venules, and an oxidative burst. In the case of an overstimulated host immune response, not only devastating respiratory symptoms but even systemic or multiorgan involvement may be observed.
Early-stage medical interventions may assist in returning the exaggerated immune response to a normal range; however, some therapeutic delay might result in excessive tissue damages, occasionally mimicking a systemic disease with a detrimental outcome.
新型冠状病毒 SARS-CoV-2 引起的大流行对科学家和医生都提出了挑战，需要他们迅速开发并紧急评估有效的诊断测试和治疗干预措施。有症状患者疾病的初始表现始终是呼吸道症状，主要症状是干咳，但越来越多的报告显示多器官受累。本文综述的目的是总结被激活吞噬细胞的肾素-血管紧张素系统在 COVID-19 发病机制中的潜在作用。
通过在 PubMed 中搜索，并使用搜索词“SARS”、“COVID-19”、“肾素-血管紧张素系统”、“吞噬细胞”、“活性自由基”、“抗氧化剂”、“ARDS”、“血栓形成”、“心肌”、“缺血”、“再灌注”、“微血管”和“ACE2”来检索相关文章的参考文献，确定了本次综述的数据。本次工作未包括会议摘要和报告。仅回顾了 1976 年至 2020 年间以英文发表的文章。
SARS 病毒的细胞靶标是血管紧张素转换酶 2，它是肾素-血管紧张素系统中的关键调节蛋白。病毒刺突蛋白消除这种酶会导致吞噬细胞过度激活，通过高内皮微静脉迁移到组织中，并发生氧化爆发。在宿主免疫反应过度刺激的情况下，不仅会出现严重的呼吸道症状，甚至可能观察到全身或多器官受累。
早期的医疗干预可能有助于将过度的免疫反应恢复到正常范围；然而，一些治疗延迟可能会导致过度的组织损伤，偶尔会出现类似全身性疾病的不良后果。
