Molecular Mechanisms of Platelet Adhesion and Activation

Dear Colleagues,

Blood coagulation, a tightly regulated biological process, prevents excessive bleeding when blood vessels are injured. Vessel injury results in the rapid accumulation of platelets at the damaged vessel site, followed by the adhesion and subsequent activation of platelets. Platelet activation triggers the release of platelets granules, further leading to the recruitment of additional platelets at the injured site to form a matured thrombus. A series of signaling events at the injured vessel site, involving the platelets, ultimately leads to the development of a clot. Coagulation results in thrombin outburst which triggers the endothelium to express P-selectin and release vWF, facilitating platelet adhesion via glycoprotein (GP) Ib-IX-V complex on the platelet membrane. Thrombin also binds to platelet GP Ib-IX-V complex, resulting in platelet activation. However, in diseased scenarios such as heart attack or stroke, platelet thrombus dissociates from the primary thrombus forming site and migrates with the blood flow to form a secondary thrombus in the coronary artery or arteries of the brain, respectively.

In the current Special Issue, we aim to expand our views in delineating the molecular mechanisms behind the adhesion and activation of platelets, whose dysregulation often contributes to the development of bleeding disorders like heart attack, stroke, etc.

Dr. Kaushik Das
Guest Editor

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• coagulation
• platelet adhesion
• platelet activation
• platelet defects
• bleeding disorders
• heart attack
• stroke
• thrombocytopenia
• clotting factors