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血小板与血管壁在血栓形成和止血中的分子相互作用。

Molecular interplay between platelets and the vascular wall in thrombosis and hemostasis.

机构信息

Phycell Group, Department of Physiology, University of Extremadura, Cáceres, 10003, Extremadura, Spain.

出版信息

Curr Vasc Pharmacol. 2013 Jul;11(4):409-30. doi: 10.2174/1570161111311040006.

Abstract

Hemostasis is an intrinsic property of the vascular system that prevents blood loss during accidental disruption of the vessel wall. Late mechanisms of hemostasis comprise vessel repair and wound healing. In contrast, the early mechanism of hemostasis comprises the quick formation of a blood cell plug, also known as thrombus, whose function is to seal the region of the vessel near the compromised surface or area. Despite the simplicity of the concept, the molecular mechanisms underlying early hemostasis are highly complex. The local rheological properties of the blood flow, the vascular region and the nature of the injury determine the mechanism of thrombogenesis. Components of the plasma, blood cells such as platelets and vascular endothelial cells are involved in thrombosis. This review focuses on platelet-vascular wall interactions during thrombosis and hemostasis and provides an overview of the main underlying molecular mechanisms.

摘要

止血是血管系统的固有特性,可防止血管壁意外破裂导致的失血。止血的晚期机制包括血管修复和伤口愈合。相比之下,止血的早期机制包括快速形成血细胞塞,也称为血栓,其功能是密封受损表面或区域附近的血管区域。尽管概念简单,但早期止血的分子机制非常复杂。血流、血管区域和损伤的局部流变学特性决定了血栓形成的机制。血浆成分、血小板等血细胞和血管内皮细胞都参与血栓形成。本文重点介绍血栓形成和止血过程中血小板与血管壁的相互作用,并概述主要的潜在分子机制。

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