Subendothelial collagen exposed to platelets after rupture of atherosclerotic plaques is the main trigger of platelet activation und acute arterial thrombotic occlusion leading to myocardial infarction or ischemic stroke. An efficacious antiplatelet therapy is essential to prevent atherothrombotic events. However, increasing potency of antiplatelet treatment is associated with an increased risk of bleeding limiting the clinical benefit for the patient since current antiplatelet strategies concomitantly affect hemostasis. Therefore, an unmet clinical need remains to develop antiplatelet strategies that selectively inhibit atherothrombosis without interfering with control of bleeding.

Platelet glycoprotein VI (GPVI) plays a crucial role in collagen-induced activation and aggregation of platelets. Since GPVI is platelet-specific and strongly involved in the pathogenesis of arterial thrombosis without great impact on normal hemostasis, GPVI moved into the focus of novel approaches of antithrombotic therapy strategies. This review summarizes ligands, properties, function and downstream signaling of GPVI and discusses the potential of GPVI as target for novel therapeutic strategies in thrombotic and inflammatory diseases on the basis of recent scientific findings and currently ongoing clinical phase I and phase II trials.

动脉粥样硬化斑块破裂后暴露于血小板的内皮下胶原蛋白是血小板活化和导致心肌梗塞或缺血性中风的急性动脉血栓闭塞的主要触发因素。有效的抗血小板治疗对于预防动脉粥样硬化血栓形成事件至关重要。然而，抗血小板治疗效力的增加与出血风险的增加相关，限制了患者的临床获益，因为目前的抗血小板策略会同时影响止血。因此，尚未满足的临床需求仍然是开发抗血小板策略，以选择性地抑制动脉粥样硬化血栓形成而不干扰出血的控制。

血小板糖蛋白 VI (GPVI) 在胶原蛋白诱导的血小板活化和聚集中起关键作用。由于 GPVI 是血小板特异性的，并且强烈参与动脉血栓形成的发病机制，而对正常止血没有太大影响，因此 GPVI 成为抗血栓治疗策略新方法的焦点。本综述总结了 GPVI 的配体、特性、功能和下游信号传导，并基于最近的科学发现和目前正在进行的 I 期和 II 期临床试验，讨论了 GPVI 作为血栓形成和炎症性疾病新治疗策略靶点的潜力。