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血管性血友病因子/ADAMTS13 失衡在 COVID-19 凝血功能障碍中的作用。

Contribution of the von Willebrand factor/ADAMTS13 imbalance to COVID-19 coagulopathy.

机构信息

Department of Bioengineering, Lehigh University, Bethlehem, Pennsylvania.

Department of Immunology and Inflammation, Centre for Haematology, Imperial College London, London, United Kingdom.

出版信息

Am J Physiol Heart Circ Physiol. 2022 Jan 1;322(1):H87-H93. doi: 10.1152/ajpheart.00204.2021. Epub 2021 Dec 10.

Abstract

The 2019 coronavirus disease (COVID-19) is the disease caused by SARS-CoV-2 infection. Although this infection has been shown to affect the respiratory system, a high incidence of thrombotic events has been observed in severe cases of COVID-19 and in a significant portion of COVID-19 nonsurvivors. Although prior literature has reported on both the coagulopathy and hypercoagulability of COVID-19, the specifics of coagulation have not been fully investigated. Observations of microthrombosis in patients with COVID-19 have brought attention to potential inflammatory endothelial injury. Von Willebrand factor (VWF) and its protease, A disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13), play an important homeostatic role in responding to endothelial injury. This report provides an overview of the literature investigating the role the VWF/ADAMTS13 axis may have in COVID-19 thrombotic events and suggests potential therapeutic strategies to prevent the progression of coagulopathy in patients with COVID-19.

摘要

2019 冠状病毒病(COVID-19)是由严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)感染引起的疾病。尽管该感染已被证明会影响呼吸系统,但在 COVID-19 的重症病例和 COVID-19 中的很大一部分死亡病例中,观察到了很高的血栓事件发生率。尽管先前的文献已经报道了 COVID-19 的凝血功能障碍和高凝状态,但凝血的具体情况尚未得到充分研究。COVID-19 患者的微血栓形成观察引起了对潜在炎症性内皮损伤的关注。血管性血友病因子(von Willebrand factor,VWF)及其蛋白酶解整合素金属蛋白酶 13(a disintegrin and metalloproteinase with a thrombospondin type 1 motif,member 13,ADAMTS13)在应对内皮损伤方面发挥着重要的动态平衡作用。本报告概述了研究 VWF/ADAMTS13 轴在 COVID-19 血栓事件中的作用的文献,并提出了潜在的治疗策略,以防止 COVID-19 患者凝血功能障碍的进展。

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