4.7 Article

Understanding COVID-19-associated coagulopathy

Journal

NATURE REVIEWS IMMUNOLOGY
Volume 22, Issue 10, Pages 639-649

Publisher

NATURE PORTFOLIO
DOI: 10.1038/s41577-022-00762-9

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Funding

  1. National Heart, Lung, and Blood Institute (NHLBI)
  2. CanVECTOR (COVID-19 Rapid Response Funding Competition)
  3. Canada Research Chairs programme
  4. Canadian Institutes of Health Research
  5. Natural Sciences and Engineering Research Council of Canada
  6. National Institutes of Health (NIH) [R01 HL142975, R01 HL104165, R35 HL135823, OT2 HL156812]

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In this article, the authors discuss the emerging understanding of COVID-19-associated coagulopathy and the need to comprehend its cellular and molecular mechanisms. They categorize the current understanding into three main pathological mechanisms and address key questions and research gaps in order to improve diagnosis and treatment. The suitability of animal models for studying this condition is also considered.
Here, the authors consider our emerging understanding of COVID-19-associated coagulopathy. They focus on the complex interactions between innate immune, coagulation and fibrinolytic pathways that can lead to potentially life-threatening thrombosis following SARS-CoV-2 infection. COVID-19-associated coagulopathy (CAC) is a life-threatening complication of SARS-CoV-2 infection. However, the underlying cellular and molecular mechanisms driving this condition are unclear. Evidence supports the concept that CAC involves complex interactions between the innate immune response, the coagulation and fibrinolytic pathways, and the vascular endothelium, resulting in a procoagulant condition. Understanding of the pathogenesis of this condition at the genomic, molecular and cellular levels is needed in order to mitigate thrombosis formation in at-risk patients. In this Perspective, we categorize our current understanding of CAC into three main pathological mechanisms: first, vascular endothelial cell dysfunction; second, a hyper-inflammatory immune response; and last, hypercoagulability. Furthermore, we pose key questions and identify research gaps that need to be addressed to better understand CAC, facilitate improved diagnostics and aid in therapeutic development. Finally, we consider the suitability of different animal models to study CAC.

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