Molecular regulation of platelet-dependent thrombosis
Molecular regulation of platelet-dependent thrombosis
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DOI：
10.1161/circulationaha.104.494468
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发表时间：
2005-10-25
期刊：
影响因子：
37.8
通讯作者：
Freedman, JE
中科院分区：
文献类型：
--
作者：
Freedman, JE
止血是一种正常的过程，可以防止出血失控后的后遗症。在某些情况下，这些相同的过程引起不良的临床事件，由于血栓闭塞的血管。大多数不稳定冠状动脉综合征是由动脉粥样硬化斑块破裂引起的，导致内膜下内容物暴露，从而引发凝血并形成富含血小板的血栓。血小板活化在导致血管闭塞的事件中的中心作用是众所周知的。然而，这个过程是复杂的，并受到无数细胞和血浆来源的介质的影响，这些介质调节闭塞性和非闭塞性血栓形成之间的平衡。
Hemostasis is a normal process preventing the sequelae of uncontrolled hemorrhage. In certain settings, these same processes cause adverse clinical events due to thrombotic occlusion of a vessel. The majority of unstable coronary syndromes result from disruption of an atherosclerotic plaque, leading to the exposure of subintimal contents, which triggers coagulation and the formation of a platelet-rich thrombus. The central role of platelet activation in the events that lead to vessel occlusion is well known. However, this process is complex and influenced by a myriad of cellular and plasma-derived mediators that regulate the balance between occlusive and nonocclusive thrombosis.