Could SARS-CoV-2 blocking of ACE2 in endothelial cells result in upregulation of CX3CL1, promoting thrombosis in COVID-19 patients?

SARS-CoV-2 is the causal agent of COVID-19 disease. Currently, infection with SARS-CoV-2 has been the cause of death of over 2.5 million people globally, and there is still no effective curative treatment. Clinically, the severe symptoms caused by COVID-19, in addition to pneumonia, are associated with the development of hyperinflammatory syndrome and thrombosis. It is urgent to expand our understanding of the molecular mechanisms involved in the pathophysiology of COVID-19. This article discusses the potential role that the chemokine CX3CL1 could have in the development of COVID-19-associated thrombosis. CX3CL1 is abundantly expressed by activated endothelium and is an important regulator of many aspects of endothelial function and dysfunction, including thrombosis. The generation of hypotheses about molecules that could be relevant in well-defined aspects of the pathophysiology of COVID-19 encourages the development of basic and clinical studies, that could help find effective and much needed treatments.