Cell-Cell Interactions in Thrombosis: Modulation of Platelet Function and Possibilities of Pharmacological Control with Aspirin.

There are several signal mechanisms involved in platelet activation, including specific receptors, G proteins, phosphatidyl inositol metabolism, synthesis of thromboxane A2 (TXA2) and other eicosanoids, changes in cytosolic calcium, and protein phosphorylation, in serine/threonine and tyrosine residues[2]. These signal mechanisms result in a conformational change in the GP IIb IIIa receptor, platelet secretion, platelet–platelet aggregation, exposure to procoagulant phospholipids in the membrane, clot retraction, and synthesis of different metabolic products.