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Activated Protein C

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Trauma Induced Coagulopathy

Abstract

Since the initial descriptions of trauma-induced coagulopathy (TIC) as a recognized clinical phenomenon, substantial efforts have been dedicated to identifying its underlying causal mechanisms. The activated protein C (APC) pathway serves as the primary anticoagulant brake on normal hemostasis, and also plays a major cytoprotective role in inflammation. Through clinical, animal model, and in vitro investigations over the past decade, the APC pathway has been implicated as a central mechanistic driver of TIC. These studies indicate that in the setting of significant tissue injury and shock, increased activation of protein C leads directly to the hypocoagulable milieu that characterizes TIC. Such findings also raise the intriguing possibility that the aberrant activation of this pathway might be susceptible to targeted therapeutic interventions to reverse or attenuate TIC. In this chapter, we will review the biology of protein C, the components and mechanisms of the protein C pathway, and the clinical importance of APC in the etiology of TIC.

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Howard, B.M., Cohen, M.J. (2016). Activated Protein C. In: Gonzalez, E., Moore, H., Moore, E. (eds) Trauma Induced Coagulopathy. Springer, Cham. https://doi.org/10.1007/978-3-319-28308-1_6

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