In platelets, VASP plays a critical role in regulating platelet activation and aggregation, which are essential steps in the formation of blood clots. VASP phosphorylation status, influenced by cyclic nucleotide-dependent kinases, determines its activity. When phosphorylated, VASP inhibits platelet aggregation, thereby acting as a negative regulator of thrombus formation. This modulation is vital for preventing inappropriate clotting while enabling normal hemostatic responses.
