Abstract
The protein C anticoagulant system plays a critical role in the regulation of haemostasis and inflammation. Binding of protein C to endothelial cell protein C receptor (EPCR) and the subsequent activation of EPCR-bound protein C by thrombin/thrombomodulin are the key steps in the protein C anticoagulant system. Activated protein C (APC) -mediated cell signalling, supported by its binding to EPCR or independent of EPCR, activates anti-inflammatory and cytoprotective pathways [1]. Therefore, pathophysiologic conditions that impair the interaction of protein C with EPCR have the potential to decrease APC generation. Such reduced binding to EPCR may not only contribute to thrombotic disorders, but also result in the loss of endogenous APC-mediated cytoprotection..
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