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Stabilin‐2 deficiency increases thrombotic burden and alters the composition of venous thrombi in a mouse model

Stabilin‐2 is an endocytic scavenger receptor that mediates the clearance of glycosaminoglycans, phosphatidylserine‐expressing cells, and the von Willebrand factor‐factor VIII (FVIII) complex. In a genome‐wide screening study, pathogenic loss‐of‐function variants in the human STAB2 gene associated with an increased incidence of unprovoked venous thromboembolism (VTE). However, the specific mechanism(s) by which stabilin‐2 deficiency influences the pathogenesis of VTE is unknown.