Department of Chemical Pathology, Faculty of Medicine, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
J Mol Cell Cardiol. 2022 Mar;164:69-82. doi: 10.1016/j.yjmcc.2021.11.010. Epub 2021 Nov 24.
The global propagation of SARS-CoV-2 leads to an unprecedented public health emergency. Despite that the lungs are the primary organ targeted by COVID-19, systemic endothelial inflammation and dysfunction is observed particularly in patients with severe COVID-19, manifested by elevated endothelial injury markers, endotheliitis, and coagulopathy. Here, we review the clinical characteristics of COVID-19 associated endothelial dysfunction; and the likely pathological mechanisms underlying the disease including direct cell entry or indirect immune overreactions after SARS-CoV-2 infection. In addition, we discuss potential biomarkers that might indicate the disease severity, particularly related to the abnormal development of thrombosis that is a fatal vascular complication of severe COVID-19. Furthermore, we summarize clinical trials targeting the direct and indirect pathological pathways after SARS-CoV-2 infection to prevent or inhibit the virus induced endothelial disorders.
新冠病毒在全球的传播导致了一场前所未有的公共卫生紧急事件。尽管肺部是 COVID-19 的主要靶器官，但在重症 COVID-19 患者中观察到全身内皮炎症和功能障碍，表现为内皮损伤标志物升高、血管内皮炎和凝血异常。在这里，我们回顾了 COVID-19 相关内皮功能障碍的临床特征；以及 COVID-19 发病的可能病理机制，包括 SARS-CoV-2 感染后的直接细胞进入或间接免疫过度反应。此外，我们讨论了可能的生物标志物，这些标志物可能表明疾病的严重程度，特别是与血栓形成的异常发展有关，血栓形成是 COVID-19 重症患者的一种致命血管并发症。此外，我们总结了针对 SARS-CoV-2 感染后直接和间接病理途径的临床试验，以预防或抑制病毒引起的内皮紊乱。
