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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, and 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. COVID-19, caused by the SARS-CoV-2 virus, drives dysregulation of angiotensin signaling, which, in turn, increases thrombin-mediated and purinergic-mediated activation of platelets and increase in inflammation. This thromboinflammation impacts the lungs and can also have systemic effects. Inhibitors of receptors that drive platelet activation or inhibitors of the coagulation cascade provide opportunities to treat COVID-19 thromboinflammation. <\/jats:p>","DOI":"10.1152\/physrev.00035.2020","type":"journal-article","created":{"date-parts":[[2020,10,30]],"date-time":"2020-10-30T13:55:02Z","timestamp":1604066102000},"page":"545-567","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":90,"title":["Inflammation and thrombosis in COVID-19 pathophysiology: proteinase-activated and purinergic receptors as drivers and candidate therapeutic targets"],"prefix":"10.1152","volume":"101","author":[{"given":"Krishna","family":"Sriram","sequence":"first","affiliation":[{"name":"Department of Pharmacology, University of California San Diego, La Jolla, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul A.","family":"Insel","sequence":"additional","affiliation":[{"name":"Department of Pharmacology 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