Deng Hai, Tang Ting-Xuan, Chen Deng, Tang Liang-Sheng, Yang Xiang-Ping, Tang Zhao-Hui
Division of Trauma & Surgical Critical Care, Department of Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Class 1901, School of Medicine, Wuhan University of Science and Technology, Wuhan 430065, China.
Pathogens. 2021 May 11;10(5):582. doi: 10.3390/pathogens10050582.
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), has been recently considered a systemic disorder leading to the procoagulant state. Preliminary studies have shown that SARS-CoV-2 can infect endothelial cells, and extensive evidence of inflammation and endothelial dysfunction has been found in advanced COVID-19. Endothelial cells play a critical role in many physiological processes, such as controlling blood fluidity, leukocyte activation, adhesion, platelet adhesion and aggregation, and transmigration. Therefore, it is reasonable to think that endothelial dysfunction leads to vascular dysfunction, immune thrombosis, and inflammation associated with COVID-19. This article summarizes the association of endothelial dysfunction and SARS-CoV-2 infection and its therapeutic strategies.
2019冠状病毒病(COVID-19)由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引起,最近被认为是一种导致促凝状态的全身性疾病。初步研究表明,SARS-CoV-2可感染内皮细胞,并且在晚期COVID-19中已发现炎症和内皮功能障碍的广泛证据。内皮细胞在许多生理过程中起关键作用,如控制血液流动性、白细胞激活、黏附、血小板黏附和聚集以及迁移。因此,有理由认为内皮功能障碍会导致与COVID-19相关的血管功能障碍、免疫血栓形成和炎症。本文总结了内皮功能障碍与SARS-CoV-2感染的关联及其治疗策略。