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COVID-19, microangiopathy, hemostatic activation, and complement
Wen-Chao Song, Garret A. FitzGerald
Wen-Chao Song, Garret A. FitzGerald
Published May 27, 2020
Citation Information: J Clin Invest. 2020;130(8):3950-3953. https://doi.org/10.1172/JCI140183.
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COVID-19, microangiopathy, hemostatic activation, and complement

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Abstract

Authors

Wen-Chao Song, Garret A. FitzGerald

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Figure 1

Potential mechanisms of complement-mediated pathology in COVID-19.

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Potential mechanisms of complement-mediated pathology in COVID-19.
SARS–...
SARS–CoV-2 virus may directly activate the complement pathways. Damaged host tissues could also secondarily activate complement via any of the three pathways: the classical pathway, the lectin pathway, or the alternative pathway. Complement activation generates the anaphylatoxins C3a and C5a and the MAC C5ab-9. The C5a anaphylatoxin can cause neutrophil and monocyte activation, promote the formation of NET and platelet-leukocyte aggregates, and stimulate neutrophil degranulation and the release of tissue factor to trigger the extrinsic coagulation pathway. These C5a effects may contribute to a hypercoagulative state leading to VTEs and disseminated intravascular coagulation (DIC). The MAC C5b-9 can cause direct endothelial injury and platelet activation, leading to TMA. Capillary and blood vessel occlusion by TMA and VTEs eventually results in tissue ischemia and oxidant injury, contributing to multiorgan failure in COVID-19. AKI, acute kidney injury; FB, complement factor B; FD, complement factor D; P, properdin.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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