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静脉血栓形成机制的新见解。

New insights into the mechanisms of venous thrombosis.

机构信息

Division of Hematology/Oncology, Department of Medicine, UNC McAllister Heart Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.

出版信息

J Clin Invest. 2012 Jul;122(7):2331-6. doi: 10.1172/JCI60229. Epub 2012 Jul 2.

Abstract

Venous thrombosis is a leading cause of morbidity and mortality in industrialized countries, especially in the elderly. Many risk factors have been identified for venous thrombosis that alter blood flow, activate the endothelium, and increase blood coagulation. However, the precise mechanisms that trigger clotting in large veins have not been fully elucidated. The most common site for initiation of the thrombus appears to be the valve pocket sinus, due to its tendency to become hypoxic. Activation of endothelial cells by hypoxia or possibly inflammatory stimuli would lead to surface expression of adhesion receptors that facilitate the binding of circulating leukocytes and microvesicles. Subsequent activation of the leukocytes induces expression of the potent procoagulant protein tissue factor that triggers thrombosis. Understanding the mechanisms of venous thrombosis may lead to the development of new treatments.

摘要

静脉血栓形成是工业化国家发病率和死亡率的主要原因,尤其是在老年人中。已经确定了许多会改变血流、激活内皮细胞并增加血液凝固的静脉血栓形成的风险因素。然而,引发大静脉内血栓形成的确切机制尚未完全阐明。血栓形成的最常见起始部位似乎是由于其倾向于缺氧的瓣膜窦窝。缺氧或炎症刺激激活内皮细胞会导致表面表达黏附受体,从而促进循环白细胞和微囊泡的结合。随后白细胞的激活诱导表达强效促凝蛋白组织因子,从而引发血栓形成。了解静脉血栓形成的机制可能会导致新的治疗方法的发展。

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