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调节血栓生长和稳定性,以实现对损伤的最佳反应。

Regulating thrombus growth and stability to achieve an optimal response to injury.

机构信息

Department of Medicine and Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.

出版信息

J Thromb Haemost. 2011 Jul;9 Suppl 1(Suppl 1):66-75. doi: 10.1111/j.1538-7836.2011.04364.x.

DOI:10.1111/j.1538-7836.2011.04364.x
PMID:21781243
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3422128/
Abstract

An optimal platelet response to injury can be defined as one in which blood loss is restrained and haemostasis is achieved without the penalty of further tissue damage caused by unwarranted vascular occlusion. This brief review considers some of the ways in which thrombus growth and stability can be regulated so that an optimal platelet response can be achieved in vivo. Three related topics are considered. The first focuses on intracellular mechanisms that regulate the early events of platelet activation downstream of G protein coupled receptors for agonists such as thrombin, thromboxane A(2) and ADP. The second considers the ways in which signalling events that are dependent on stable contacts between platelets can influence the state of platelet activation and thus affect thrombus growth and stability. The third focuses on the changes that are experienced by platelets as they move from their normal environment in freely-flowing plasma to a very different environment within the growing haemostatic plug, an environment in which the narrowing gaps and junctions between platelets not only facilitate communication, but also increasingly limit both the penetration of plasma and the exodus of platelet-derived bioactive molecules.

摘要

理想的血小板反应可定义为

在限制失血和实现止血的同时,不会因不必要的血管阻塞而导致进一步的组织损伤。本综述简要讨论了一些调节血栓形成和稳定性的方法,以便在体内实现理想的血小板反应。考虑了三个相关的主题。第一个主题集中在调节血小板激活早期事件的细胞内机制上,这些机制涉及到血小板激活的 G 蛋白偶联受体激动剂,如凝血酶、血栓烷 A2 和 ADP。第二个主题考虑了依赖于血小板稳定接触的信号事件如何影响血小板激活状态,从而影响血栓形成和稳定性。第三个主题集中在血小板从正常的自由流动血浆环境转移到正在形成的止血塞中的非常不同的环境时所经历的变化,在这个环境中,血小板之间的间隙和连接不仅促进了通讯,而且越来越限制了血浆的渗透和血小板衍生的生物活性分子的外流。

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本文引用的文献

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Towards standardization of in vivo thrombosis studies in mice.迈向小鼠体内血栓形成研究的标准化。
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Diminished contact-dependent reinforcement of Syk activation underlies impaired thrombus growth in mice lacking Semaphorin 4D.Sema4D 缺失小鼠中 Syk 激活的接触依赖性增强减弱,导致血栓生长受损。
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Platelet endothelial cell adhesion molecule-1 regulates collagen-stimulated platelet function by modulating the association of phosphatidylinositol 3-kinase with Grb-2-associated binding protein-1 and linker for activation of T cells.血小板内皮细胞黏附分子-1 通过调节与 Grb2 相关结合蛋白-1 和 T 细胞激活连接蛋白的磷酸肌醇 3-激酶的关联来调节胶原刺激的血小板功能。
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The final steps of integrin activation: the end game.整合素激活的最后步骤:终局。
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