Figure 1.

Platelet adhesion, activation, aggregation. When blood vessels are damaged, platelets become activated and attach to the site of damage. This is facilitated by GPIbα and vWF, acting as “tether” and allowing other molecules such as GPVI to interact with collagen. This triggers a series of events that convert integrins on the surface of platelets to a high-affinity state and release ADP and TXA2, further activating platelets and promoting forming a stable blood clot. The tissue factor released from the damaged tissue activates thrombin, causing integrin GPIIb/IIIa to bind with fibrinogen and vWF, further strengthening the attachment of platelets and contributing to the formation of a stable blood clot.