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Comment
. 2020 Aug;7(8):e553-e555.
doi: 10.1016/S2352-3026(20)30215-5. Epub 2020 Jun 30.

Endothelial cells orchestrate COVID-19 coagulopathy

Jamie M O'Sullivan  1 , Dennis Mc Gonagle  2 , Soracha E Ward  1 , Roger J S Preston  1 , James S O'Donnell  3
Affiliations
Comment

Endothelial cells orchestrate COVID-19 coagulopathy

Jamie M O'Sullivan et al. Lancet Haematol. 2020 Aug.
No abstract available

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Figures

Figure
Figure
Endotheliopathy in COVID-19 coagulopathy The healthy alveolus and pulmonary vasculature exist in close anatomical juxtaposition, and thrombosis is prevented by the endothelial cell monolayer that expresses surface thrombomodulin. Endothelial cell activation and damage are triggered though multiple pathways, including pro-inflammatory cytokines, hypoxia, complement activation, and NETosis. As a result of this activation, Weibel-Palade body exocytosis from endothelial cells is triggered resulting in the release of ultra-large VWF multimers and P-selectin; released VWF binds to platelets, neutrophils, and monocytes to initiate microvascular thrombosis. Concurrently, thrombomodulin is shed from endothelial cell surfaces, which further promotes a procoagulant and pro-inflammatory local milieu within the pulmonary vasculature. Finally, endothelial cell damage results in separation from the basement membrane and loss of tight junctions, enhancing vascular permeability. NETosis=neutrophil extracellular trap activation and release. PAI-1= plasminogen activator inhibitor-1. SARS-CoV-2=severe acute respiratory syndrome coronavirus 2. VWF=von Willebrand factor.
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