Figure 1.

Thromboxane‐mediated platelet activation. At sites of vascular injury, von Willebrand factor (VWF) binds platelet adhesion receptor glycoprotein (GP)Ibα. Subsequent phosphorylation of P38 mitogen activated protein kinase (MAPK) and cytosolic phospholipase A2 (cPLA₂) leads to the liberation of arachidonic acid (AA) from the phospholipid bilayer. Similar to VWF binding, AA is also released following stimulation of platelets by other agonists. AA is converted into thromboxane (Tx)A₂ by cyclo‐oxygenase 1 (COX‐1) activity. TxA₂ amplifies platelet aggregation by binding to its receptor TPα in a positive feedback loop. NSAID including aspirin inhibit COX‐1 activity and thereby inhibit platelet aggregation