Platelets in Thrombosis and Hemostasis: Old Topic with New Mechanisms

摘要: Platelets are small anucleate cells generated from megakaryocytes in the bone marrow. After being released into circulation, platelets play key roles surveillance of vascular injury, and can quickly adhere aggregate at the site which critical events for repair hemostasis. However, same biological processes of platelet adhesion aggregation may also cause thrombotic disorders. The formation a platelet plug at sites of atherosclerotic lesion rupture is most common mechanism leading to myocardial or cerebral infarction. Platelet-related deep vein thrombosis one causes mortality worldwide. contribution several platelet receptors their ligands has been highlighted these processes. In adhesion, particularly high shear stress, GPIbα-von Willebrand factor (VWF) interaction initiate this event, followed by GPVI signalling firm platelet mediated members integrin family, such as β3 (αIIbβ3) β1 (α2β1, α5β1) integrins. In platelet aggregation, although GPIbα-VWF, P selectin-sulfatides, other molecules, be involved, process is mainly its ligands, fibrinogen VWF. It intriguing that platelet adhesion still occur mice lacking both VWF, suggesting unforeseen molecule(s) important Identification characterization molecules will enrich our knowledge basic science hemostasis thrombosis, lead development new therapies against bleeding disorders diseases.