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Updated: Oct 29, 2026

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
Published on: August 14, 2017
The role of VWF/ADAMTS13 axis in COVID-19-associated coagulopathy
Quan Zhang1,2, Ye Tan3, Meijuan Peng1
1Department of Pulmonary and Critical Care Medicine, The Tenth Affiliated Hospital of Southern Medical University (Dongguan People's Hospital), Dongguan, Guangdong, China.
Abstract:
Coronavirus disease 2019, which broke out in 2019, is a disease caused by SARS-CoV-2 infection. Although this infection mainly affects the respiratory system, a high incidence of thrombotic events has been observed in severe or critically ill cases and in a considerable number of non-survivors of COVID-19. Although the coagulation dysfunction and hypercoagulability of COVID-19 have been reported in the literature, the specific situation of its coagulation function has not been fully studied. The observation of microvascular thrombosis in COVID-19 patients has attracted our attention to investigate the potential inflammatory endothelial injury or damage. Von Willebrand factor (VWF) and its proteolytic protease, A Disintegrin And Metalloproteinase with ThromboSpondin type 1 motifs, 13 (ADAMTS13), play an important role in maintaining the vascular health and organ perfusion. Therapeutic and prophylactic anticoagulation are important measures to prevent these kinds of thrombotic events, but new treatments such as recombinant ADAMTS13 and anti-VWF nanobody Caplacizumab are being studied in vitro for thrombosis with high efficacy. This review focuses on the discussion of the current research progress of the treatment of COVID-19-associated coagulopathy by correcting the imbalance of VWF-ADAMTS13 axis, the existing problems, and the prospects.
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