Abstract
In response to blood vessel injury, circulating platelets interact with the exposed subendothelial matrix, which triggers platelet activation, adhesion, and aggregation, leading to the formation of a hemostatic plug to prevent blood loss. This process is essential for normal hemostasis but can lead to the formation of pathological thrombi, resulting in cardiovascular diseases such as heart attack or stroke. The initial stages of platelet adhesion depend on the binding of the GPIb-IX-V complex on the platelet surface to immobilize von Willebrand factor (VWF) at the exposed subendothelial connective tissue (1,2).
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