Harnessing the Platelet Signaling Network to Produce an Optimal Hemostatic Response

被引:22
作者
Brass, Lawrence F. [1 ]
Tomaiuolo, Maurizio [1 ]
Stalker, Timothy J. [1 ]
机构
[1] Univ Penn, Perelman Sch Med, Dept Med, Philadelphia, PA 19104 USA
关键词
Platelets; Hemostasis; Vascular injury; Signal transduction; Networks; G protein-coupled receptors; G proteins; Integrins; GLYCOPROTEIN IB-ALPHA; PROTEIN-TYROSINE-PHOSPHATASE; CYTOSOLIC PHOSPHOLIPASE A(2); STIMULATED HUMAN PLATELETS; ACTIVATED RECEPTORS 1; G(I) FAMILY MEMBERS; THROMBIN-RECEPTOR; ADP RECEPTORS; SHAPE CHANGE; P2X(1) RECEPTORS;
D O I
10.1016/j.hoc.2013.02.002
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Once released into the circulation by megakaryocytes, circulating platelets can undergo rapid activation at sites of vascular injury and resist unwarranted activation, which can lead to heart attacks and strokes. Historically, the signaling mechanisms underlying the regulation of platelet activation have been approached as a collection of individual pathways unique to agonist. This review takes a different approach, casting platelet activation as the product of a signaling network, in which activating and restraining mechanisms interact in a flexible network that regulates platelet adhesiveness, cohesion between platelets, granule secretion, and the formation of a stable hemostatic thrombus.
引用
收藏
页码:381 / +
页数:30
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