Brass Lawrence F, Zhu Li, Stalker Timothy J
University of Pennsylvania, Department of Medicine, Division of Hematology-Oncology, Philadelphia, PA 19104, USA.
Arterioscler Thromb Vasc Biol. 2008 Mar;28(3):s43-50. doi: 10.1161/ATVBAHA.107.161026. Epub 2008 Jan 3.
Platelet activation in vivo can be part of the hemostatic response to injury or a pathological response to disease. In either setting, platelets adhere to the vessel wall and to each other, forming a closely packed mass interspersed with fibrin. Recent studies have identified new molecules on the platelet surface and within platelets that support and regulate thrombus growth and stability, ensuring that platelet accumulation after injury is sufficient to stop bleeding, but not so exuberant that vascular occlusion occurs. An understanding of how this balance is achieved helps to illuminate the events of platelet activation and, at the same time, provides potential targets for new classes of antiplatelet agents.
体内血小板活化可能是对损伤的止血反应的一部分,也可能是对疾病的病理反应。在这两种情况下,血小板都会黏附于血管壁并相互黏附,形成一个紧密堆积的团块,其间散布着纤维蛋白。最近的研究已经在血小板表面和血小板内发现了新的分子,这些分子支持并调节血栓的生长和稳定性,确保损伤后血小板的聚集足以止血,但又不会过于旺盛以至于发生血管阻塞。了解这种平衡是如何实现的,有助于阐明血小板活化的过程,同时也为新型抗血小板药物提供了潜在靶点。