Dysregulated platelet function in COVID-19 patients

More than two year-experience in monitoring patients with severe novel coronavirus disease revealed an increased risk of macroand microcirculatory thrombosis, clinically manifested by heart attack, stroke, thromboses of rare localizations (thrombosis of the hepatic veins, mesenteric veins, cerebral sinuses, portal vein), being the main cause of adverse outcomes. Thromboembolic complications, expressed as sepsis-induced coagulopathy, disseminated intravascular coagulation, venous and arterial thromboembolism, pulmonary embolism, microthrombosis, and thrombotic microangiopathy were noted to affect various organs such as the lungs, heart, kidneys, and brain. Earlier, we showed that hypercoagulability is closely related to inflammatory diseases and hemostasis dysregulation. Endothelial injury and dysfunction have been identified as critical pathways to thrombosis, and other mechanisms occurring in the microvasculature were described such as endothelial activation, cytokine storm, and formation of neutrophil extracellular traps (NETs). However, a role of platelets in severe COVID-19 has not been examined. Platelets are small non-nucleated cells most known as the central mediators of hemostasis. However, upon activation, platelets release a variety of immunomodulatory cytokines and chemokines involved in regulating immune response. Because platelets are involved in both immunity and coagulation, they play a central role in immunothrombosis, a physiological process wherein immune cells induce microthrombogenesis both to prevent spread of pathogens and facilitate their clearance. Moreover, platelets can directly interact with viral receptors including those related to SARS-CoV-2. Platelet dysfunction includes both thrombocytopenia and platelet hyperactivation. It should be noted that persistent thrombocytopenia is usually correlated with mortality being associated with thrombosis of the cerebral sinuses, splanchnic system, autoimmune reactions, as well as with administered heparin and vaccines. Therefore, here we review a role of platelets in the pathogenesis of COVID-19.

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