Hemostatic and signaling functions of transfused platelets

Metabolic studies have revealed a gradual impairment in platelet integrity during storage, a process termed the platelet storage lesion. Recent evidence shows that stored platelets also lose signaling responses to physiological agonists with impaired integrin activation, secretion, and aggregation of the cells. On the other hand, storage leads to a gain in platelet activation properties, such as release of microparticles and appearance of surface epitopes for their clearance by macrophages. New techniques for measuring flow-induced thrombus formation and platelet-dependent coagulation provide evidence that the hemostatic activity of platelets decreases during storage. Besides pharmacological inhibition, novel storage strategies, like metabolic suppression, should be considered to better preserve platelet functionality while limiting the expression of clearance markers. Understanding the changes that occur in association with the platelet storage lesion and the use of updated storage methods will help to generate platelets for transfusion with optimal hemostatic function and a long circulation time after transfusion.