The glycoprotein Ib-IX-V complex in platelet adhesion and signaling
The glycoprotein Ib-IX-V complex in platelet adhesion and signaling
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DOI：
10.1055/s-0037-1615854
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发表时间：
1999-08-01
影响因子：
6.7
通讯作者：
Berndt, MC
中科院分区：
文献类型：
--
作者：
Andrews, RK;Shen, Y;Berndt, MC
血栓形成可导致不稳定型心绞痛、急性心肌梗死或中风，这些都是西方世界的主要死亡原因。循环中的血小板粘附并形成闭塞性血栓，这可能是由于斑块破裂后暴露于硬化病变，也可能是由于阻塞冠状动脉中的病理性剪切应力。这一过程与正常的止血过程相似，即血小板粘附在血管损伤部位的内皮下，被激活，并招募额外的血小板形成血栓。在高剪切下，血栓形成由特异性血小板膜粘附受体（糖蛋白（GP）Ib-IX-V复合物）引发，所述糖蛋白（GP）Ib-IX-V复合物结合血管壁或血浆中的粘附糖蛋白（von Willebrand因子（vWF））。最近的证据还表明，血小板粘附内皮细胞和白细胞可能参与动脉粥样硬化，血栓形成和炎症。初步研究结果表明，GP Ib-IX-V特异性识别P-选择素，选择素超家族的一个成员，这种相互作用可能至少部分地调节血小板-内皮细胞粘附。本文综述了GP Ib-IX-V构效关系的最新研究进展。
Thrombosis can result in unstable angina, acute myocardial infarction, or stroke, all major causes of death in the Western world. Circulating platelets become adherent and form an occlusive thrombus, either by exposure to sclerotic lesions following plaque rupture or in response to pathological shear stress in obstructed coronary arteries. This process parallels normal haemostasis, where platelets adhere to the subendothelium at sites of vascular injury, become activated, and recruit additional platelets to the developing thrombus. At high shear, thrombus formation is initiated by a specific platelet membrane adhesion receptor, the glycoprotein (GP) Ib-IX-V complex, which binds the adhesive glycoprotein, von Willebrand factor (vWF), in the vessel wall or plasma. Recent evidence also suggests that platelet adhesion to endothelial cells and leukocytes may be involved in atherogenesis, thrombosis, and inflammation. Preliminary findings indicate that GP Ib-IX-V specifically recognizes P-selectin, a member of the selectin superfamily, an interaction that may, at least partially, regulate platelet-endothelial cell adhesion. This review focuses on recent advances in understanding structure-activity relationships of GP Ib-IX-V.