Contribution of the von Willebrand factor/ADAMTS13 imbalance to COVID-19 coagulopathy
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. A...
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Published in | American journal of physiology. Heart and circulatory physiology Vol. 322; no. 1; pp. H87 - H93 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
United States
American Physiological Society
01.01.2022
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Series | Vascular Biology and Microcirculation |
Subjects | |
Online Access | Get full text |
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Summary: | 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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-2 |
ISSN: | 0363-6135 1522-1539 |
DOI: | 10.1152/AJPHEART.00204.2021 |