Endothelial cells in ischaemic microvessels undergo necroptosis, which is linked to the activation of complement pathways, haemolysis of red blood cells (RBCs), and deposition and accumulation of haemolysed RBC membranes at the sites of endothelial cell death. Physiologically, this process might be a novel haemostatic mechanism to prevent microvascular interstitial bleeding; however, excessive RBC aggregation can cause microvascular obstruction and might contribute to the microangiopathy that is a central feature of coronavirus disease 2019 (COVID-19) and other ischaemic conditions. These findings were published in Nature.
Shaun Jackson and colleagues set out to investigate further the endotheliopathy that occurs in COVID-19. Analysis of endothelial cells from patients with COVID-19 indicated that endothelial cell death was a prominent feature. Histological analysis revealed the deposition of haemolysed RBCs at the sites of endothelial cell death. Of note, this process did not involve fibrin or platelets and was not linked to coagulopathy. In patients with COVID-19, haemolysed RBC membranes were found to be the dominant cause of microvascular obstruction in the heart, kidneys and liver (but, interestingly, not the lungs).
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