PMC:7386875 / 45535-47319 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7386875","sourcedb":"PMC","sourceid":"7386875","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7386875","text":"Targeting Thrombosis for the Treatment of COVID-19\nThe high rates of thrombotic complications observed in patients with severe COVID-19, combined with the current lack of an effective therapy for SARS-CoV-2, has led to significant interest regarding the use of antithrombotics for patients with COVID-19. In this regard, antithrombotic drugs which possess anti-inflammatory and/or antiviral properties have already entered clinical trials and will be discussed below (Figure 4).\nFigure 4. Treatments for targeting coronavirus disease 2019 (COVID-19)-associated thrombosis. Heparins, including unfractionated heparin (UFH) and low molecular weight heparin (LMWH), bind antithrombin (AT), and potentiate the inhibitory effect of AT on coagulation factors Xa and thrombin. Furthermore, UFH may have antiviral effects by having the ability to bind the receptor-binding domain of the S protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in addition to potentially acting as a decoy for naturally expressed heparan sulfate thus reducing the ability of the virus to bind to and invade cells. The putative anti-inflammatory effects of UFH is related to its ability to bind danger-associated molecular pattern (DAMPs). Inhibitors of FXII block the contact factor pathway of coagulation, initiated by NETs, and also appear to have pleiotropic anti-inflammatory effects. Antiplatelet agents, such as dipyridamole, nafamostat, and aspirin inhibit platelet activation, which can inhibit NETosis and the release of platelet-derived DAMPs such as HMGB (high mobility group box)-1. Nafamostat may inhibit the TMPRSS-2 (transmembrane protease serine 2) and therefore impede viral entry. Fibrinolytics, such as tPA (tissue-type plasminogen activator), degrade cross-linked 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