激动剂诱导血小板活化机制及抗血小板药物研究进展

血小板在凝血酶、胶原、血小板活化因子、花生四烯酸、二磷酸腺苷、肾上腺素及5-羟色胺等激动剂作用下产生一系列复杂的信号转导，可引起血小板包括形变、颗粒内容物释放、聚集等生理反应。血小板在血管损伤部位的活化聚集是正常凝血的关键步骤之一，但过度的血小板聚集会形成血栓，从而引发急性缺血事件。因此，抗血小板治疗是血栓性疾病治疗的重要方向之一。目前的抗血小板药物主要针对活化通路中的受体或者信号分子，通过抑制受体或者阻断信号传播而发挥作用。本文对常见诱导剂诱导血小板活化的靶点和作用机制进行介绍，并对受体拮抗药和其他抗血小板药物进行综述，为进一步研究抗血小板药物提供参考。

Mechanism of agonist-induced platelet activation and research progress of anti-platelet drugs

Thrombin, collagen, platelet activating factor, arachidonic acid, adenosine diphosphate, adrenaline, serotonin and other platelet agonists can stimulate platelet to generate a series of complex signal transduction and then cause platelet physiological responses including deformation, granule release and aggregation etc. Although platelet activation and aggregation at sites of vascular injury is an essential step in coagulation process, excessive platelet accumulation leads to the formation of occlusive thrombi, which are responsible for acute ischemic events. Therefore, anti-platelet therapy is an important approach for the treatment of thrombotic diseases. Currently used anti-platelet drugs, which primarily act through receptors and/or signaling molecules in activation pathways, achieving their effects by inhibiting platelet receptors or blocking signal transmission. In this review, the targets of the above-mentioned platelet agonists and their specific activation mechanisms are introduced; receptor antagonists and other anti-platelet drugs are also summarized.