Abstract
The 2019 coronavirus disease (COVID-19) is the disease caused by SARS-CoV-2 infection. While 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 non-survivors. While 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 COVID-19 patients 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 COVID-19 patients.
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CITATION STYLE
Seth, R., McKinnon, T. A. J., & Zhang, X. F. (2022). Contribution of the von Willebrand Factor/ADAMTS13 Imbalance to COVID-19 Coagulopathy. American Journal of Physiology - Heart and Circulatory Physiology, 322(1), 1–20. https://doi.org/10.1152/AJPHEART.00204.2021
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