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?:abstract
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Evolving information has identified disease mechanisms and dysregulation of host biology that might be targeted therapeutically in COVID-19. Thrombosis and coagulopathy, associated with pulmonary injury and inflammation, are emerging clinical features of COVID-19. We present a framework for mechanisms of thrombosis in COVID-19 that initially derive from interaction of SARS-CoV-2 with ACE2, resulting in dysregulation of angiotensin signaling and subsequent inflammation and tissue injury. These responses result in increased signaling by thrombin (proteinase-activated) and purinergic receptors, which promote platelet activation and exert pathological effects on other cell types (e.g., endothelial cells, epithelial cells, fibroblasts), further enhancing inflammation and injury. Inhibitors of thrombin and purinergic receptors may thus have therapeutic effects by blunting platelet-mediated thromboinflammation and dysfunction in other cell types. Such inhibitors include agents (e.g., anti-platelet drugs) approved for other indications and that could be repurposed to treat, and potentially improve the outcome of, COVID-19 patients.
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