Endothelial activation and dysfunction in COVID-19: from basic mechanisms to potential therapeutic approaches.
Endothelial activation and dysfunction in COVID-19: from basic mechanisms to potential therapeutic approaches.
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DOI：
10.1038/s41392-020-00454-7
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发表时间：
2020-12-24
影响因子：
39.3
通讯作者：
Duan G
中科院分区：
文献类型：
--
作者：
Jin Y;Ji W;Yang H;Chen S;Zhang W;Duan G
于二零二零年三月十二日，世界卫生组织宣布2019冠状病毒病（COVID-19）爆发为大流行。截至2020年8月4日，全球已报告超过1800万例确诊感染。大多数患者症状轻微，但部分患者出现呼吸衰竭，这是COVID-19患者死亡的主要原因。血管紧张素转换酶2高表达的内皮细胞是炎症反应和凝血的主要参与者和调节者。越来越多的证据表明，内皮激活和功能障碍通过改变血管屏障的完整性、促进促凝状态、诱导内皮炎症甚至介导白细胞浸润参与COVID-19的发病机制。本文综述了COVID-19期间内皮激活和功能障碍的细胞和分子机制，强调了主要介质和治疗意义。
On 12 March 2020, the outbreak of coronavirus disease 2019 (COVID-19) was declared a pandemic by the World Health Organization. As of 4 August 2020, more than 18 million confirmed infections had been reported globally. Most patients have mild symptoms, but some patients develop respiratory failure which is the leading cause of death among COVID-19 patients. Endothelial cells with high levels of angiotensin-converting enzyme 2 expression are major participants and regulators of inflammatory reactions and coagulation. Accumulating evidence suggests that endothelial activation and dysfunction participate in COVID-19 pathogenesis by altering the integrity of vessel barrier, promoting pro-coagulative state, inducing endothelial inflammation, and even mediating leukocyte infiltration. This review describes the proposed cellular and molecular mechanisms of endothelial activation and dysfunction during COVID-19 emphasizing the principal mediators and therapeutic implications.
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影响因子：
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作者：
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通讯作者：
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DOI：
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