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Updated: Jul 21, 2025

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The APC-EPCR-PAR1 axis in sickle cell disease.

Nirupama Ramadas1, Erica M Sparkenbaugh1,2

  • 1Department of Medicine, Blood Research Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.

Frontiers in Medicine
|July 27, 2023
PubMed
Summary

Sickle Cell Disease involves red blood cell sickling due to abnormal hemoglobin. This review explores how protease-activated receptor 1 (PAR1) activation by thrombin and activated protein C (APC) impacts the disease.

Keywords:
activated protein C (APC)endothelial protein C receptor (EPCR)inflammationprotease activated receptor 1 (PAR1)sickle cell anemiasickle cell diseasethrombinvaso-occlusion

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Area of Science:

  • Hematology
  • Molecular Biology
  • Pathophysiology

Background:

  • Sickle Cell Disease (SCD) is an inherited blood disorder characterized by abnormal hemoglobin (HbS), leading to red blood cell sickling.
  • SCD pathologies include hemolytic anemia and vaso-occlusive episodes, with complications affecting multiple organ systems.
  • Endothelial activation, inflammation, and thrombosis are key features of SCD pathophysiology.

Purpose of the Study:

  • To review the activation of protease-activated receptor 1 (PAR1) by thrombin and activated protein C (APC).
  • To discuss the role of the APC-EPCR-PAR1 axis in Sickle Cell Disease.
  • To explore the potential therapeutic implications of targeting this axis in SCD.

Main Methods:

  • Literature review focusing on PAR1 activation pathways.
  • Analysis of the dysregulated APC system in SCD.
  • Discussion of the interplay between thrombin, APC, EPCR, and PAR1 in SCD pathogenesis.

Main Results:

  • PAR1 activation by thrombin contributes to endothelial dysfunction and inflammation in SCD.
  • Activated protein C (APC) can also activate PAR1, promoting endothelial barrier protection.
  • The APC system is dysregulated in SCD, potentially impacting PAR1-mediated signaling.

Conclusions:

  • The APC-EPCR-PAR1 axis represents a critical signaling pathway in SCD.
  • Understanding this axis may reveal novel therapeutic targets for managing SCD complications.
  • Further research is warranted to elucidate the precise role of PAR1 in SCD pathophysiology.