Contribution of the von Willebrand factor/ADAMTS13 imbalance to COVID-19 coagulopathy
Contribution of the von Willebrand factor/ADAMTS13 imbalance to COVID-19 coagulopathy
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冯·维勒布兰德因子/ADAMTS13 失衡对 COVID-19 凝血病的影响
DOI：
10.1152/ajpheart.00204.2021
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发表时间：
2022
影响因子：
4.8
通讯作者：
Zhang, X. Frank
中科院分区：
文献类型：
--
作者：
Seth, Ryan;McKinnon, Thomas A.;Zhang, X. Frank
2019冠状病毒病（COVID-19）是由SARS-CoV-2感染引起的疾病。虽然这种感染已被证明会影响呼吸系统，但在COVID-19严重病例和很大一部分COVID-19非幸存者中观察到血栓形成事件的高发。虽然先前的文献报道了COVID-19的凝血功能障碍和高凝性，但凝血的具体情况尚未得到充分研究。COVID-19患者微血栓形成的观察引起了人们对潜在炎症性内皮损伤的关注。血管性血友病因子（VWF）及其蛋白酶，一种具有血小板反应蛋白1型motif的崩解素和金属蛋白酶，成员13 (ADAMTS13)，在内皮损伤反应中发挥重要的稳态作用。本报告概述了研究VWF/ADAMTS13轴在COVID-19血栓形成事件中可能起作用的文献，并提出了预防COVID-19患者凝血功能障碍进展的潜在治疗策略。
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.
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