SARS-CoV-2 and endothelial cell interaction in COVID-19: molecular perspectives.
SARS-CoV-2 and endothelial cell interaction in COVID-19: molecular perspectives.
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DOI：
10.1530/vb-20-0017
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Pintus G
中科院分区：
文献类型：
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作者：
Giordo R;Paliogiannis P;Mangoni AA;Pintus G
SARS-CoV-2是导致冠状病毒疾病（COVID-19）的病原体，该疾病已被世界卫生组织宣布为大流行病。COVID-19的临床演变从无症状感染到死亡。老年人和患有基础疾病的患者，特别是糖尿病、心血管和慢性呼吸道疾病的患者更容易患上严重的COVID-19。据报道，COVID-19导致了显著的内皮损伤，越来越多的证据支持这种改变在疾病发作和进展中的关键病理生理作用。特别是，继发于内皮及其主要成分内皮细胞的结构和功能损伤的血管稳态受损，导致了在COVID-19患者中观察到的全身促炎状态和多器官受累。本文综述了支持内皮细胞是SARS-CoV-2的关键靶点这一观点的现有证据，并重点介绍了SARS-CoV-2与内皮细胞相互作用的分子机制。
SARS-CoV-2 is the agent responsible for the coronavirus disease (COVID-19), which has been declared a pandemic by the World Health Organization. The clinical evolution of COVID-19 ranges from asymptomatic infection to death. Older people and patients with underlying medical conditions, particularly diabetes, cardiovascular and chronic respiratory diseases are more susceptible to develop severe forms of COVID-19. Significant endothelial damage has been reported in COVID-19 and growing evidence supports the key pathophysiological role of this alteration in the onset and the progression of the disease. In particular, the impaired vascular homeostasis secondary to the structural and functional damage of the endothelium and its main component, the endothelial cells, contributes to the systemic proinflammatory state and the multiorgan involvement observed in COVID-19 patients. This review summarizes the current evidence supporting the proposition that the endothelium is a key target of SARS-CoV-2, with a focus on the molecular mechanisms involved in the interaction between SARS-CoV-2 and endothelial cells.