Protein C

Abstract

Since trauma-induced coagulopathy (TIC) was first recognized as a clinical phenomenon, substantial effort has been dedicated to identifying its underlying mechanisms. The activated protein C (APC) pathway serves as the primary anticoagulant brake on normal hemostasis and plays a major cytoprotective role in inflammation. Through in vitro, animal, and clinical research over the last two decades, the APC pathway has been implicated as a central mechanistic driver of TIC. In the setting of significant tissue injury and shock, activation of protein C leads to the hypocoagulable state characteristic of TIC. Aberrant activation of this pathway might be susceptible to targeted therapeutic interventions to reverse or attenuate deranged coagulation after injury. In this chapter, we review the components and regulation of the APC pathway and its clinical role in the etiology of TIC.