The Endothelial Protein C Receptor (EPCR) is vital in regulating coagulation, inflammation, and identifying stem cells.

EPCR activation is necessary for protein C to APC conversion, crucial for anti-coagulation and controlling inflammation by inhibiting Th17 cells.

A lack of EPCR, as evidenced in gene-deleted mice, is fatal at early embryonic stages, indicating its essential role in homeostasis.

Deficiency in EPCR can lead to increased thrombin, inflammation, and immune complications, while overexpression may protect against certain injuries.

Inflammatory triggers can cause EPCR shedding from cells, potentially promoting a pro-thrombotic state due to loss of its protective effects.

Elevated levels of soluble EPCR and anti-EPCR antibodies correlate with a higher risk of thrombosis and other health issues.

Understanding the regulation of EPCR shedding and ligand interactions could offer valuable therapeutic targets for disease treatment.