Shaping the platelet response to vascular injury

被引:50
作者
Stalker, Timothy J. [1 ]
Welsh, John D. [1 ]
Brass, Lawrence F. [1 ]
机构
[1] Univ Penn, Dept Med, Perelman Sch Med, Philadelphia, PA 19104 USA
关键词
hemostasis; in-vivo models; platelets; systems biology; thrombosis; THROMBUS FORMATION; IN-VIVO; TISSUE FACTOR; PROCOAGULANT ACTIVITY; GLYCOPROTEIN-VI; CALCIUM SIGNALS; MOLECULAR-BASIS; ADP RECEPTORS; BLOOD-CLOTS; ACTIVATION;
D O I
10.1097/MOH.0000000000000070
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review Several decades of work by many investigators have elucidated the major signaling pathways responsible for platelet activation. Still to be fully understood is how these pathways are integrated into a single network and how changing conditions within a growing thrombus affect that network. In this review we will consider some of the recent studies that address these issues and describe a model that provides insights into platelet activation as it occurs in vivo. Recent findings Genetic and pharmacologic studies performed in vivo have demonstrated that platelet activation during hemostasis and thrombosis is heterogeneous. Those studies indicate that distinct platelet activation pathways are not merely redundant, but are coordinated in time and space to achieve an optimal response. This coordination is achieved at least in part by the evolving distribution of platelet agonists and changes in solute transport within a hemostatic plug. Summary Studies examining the coordination of platelet signaling in time and space continue to increase our understanding of hemostasis and thrombosis. In addition to helping to decipher platelet biology, the results have implications for the understanding of new and existing antiplatelet agents and their potential risks.
引用
收藏
页码:410 / 417
页数:8
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