HRG binds directly to platelet membrane receptors GPIbα and GPIIb/IIIa, modulating platelet function.
It competes with von Willebrand factor (VWF) and fibrinogen for receptor binding, impairing platelet adhesion and aggregation.
HRG attenuates platelet-mediated thrombus formation under high-shear conditions in vitro.
Pathological reductions of plasma HRG levels in sepsis and COVID-19 associate with a hyperreactive platelet phenotype, implicating HRG in thromboinflammatory disease modulation.
