Abstract
PAR-1-mediated the endothelial disruption that occurs in the context of thromboinflammation. In addition, PAR1 promotes a profibrotic phenotype in fibroblasts, alveolar inflammation, and apoptosis. This is an active area of research; more data are needed to clarify similarities and differences of the PARs and their modulators in Post and Critical cases of COVID-19. Such issues are especially relevant given the potential use PAR-1 as a marker of promote thrombosis and tissue injury through a proposed mechanism between inflammation and thrombosis that was reported previously. This paper would track the theoretical role of PAR-1 as a marker of promote thrombosis in COVID-19 cases by looking for the following questions: What is the Cross Talk Between Thromboinflammation and Protease-activated receptors during Post and Critical cases of COVID-19?
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