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Mechanism of Thrombin-Induced Changes in Vascular Endothelial Cell Permeability

文叶 浩
Published: 1 January 2021
Hans Journal of Biomedicine , Volume 11, pp 96-105; doi:10.12677/hjbm.2021.112013

Abstract: 完整的内皮屏障功能与机体正常的生理活动密不可分,血管内皮屏障功能受损,会出现血管渗漏、水肿等一系列病理变化,而凝血酶正是目前经典的内皮屏障功能破坏剂。从18世纪至今,人们追寻于研究凝血酶诱导内皮渗透性升高的相关机制,希望能从中找到对抗凝血酶破坏屏障功能的方法。本文将针对研究中凝血酶诱导血管内皮细胞渗透性增加的机制,包括凝血酶及其受体的相关特性,以及Ca2+、PKC、Rho GTPases家族、酪氨酸激酶/磷酸酶途径等在凝血酶诱导EC渗透性增加中的作用,结合近年来有关S1P及自噬相关通路的作用作一综述。 Intact endothelial barrier function is closely related to body physiological activities. Vascular leak-age, edema and a series of pathological changes will arise if vascular endothelial barrier function is damaged. Thrombin is the most common breaker of endothelial barrier function. Since the 18th century, researchers have investigated the mechanism of thrombin-induced increase in endothelial permeability, seeking a way to ameliorate thrombin-induced barrier disruption. This article is a summary focus on recent studies on the mechanism of thrombin inducing endothelial cell permea-bility, including the characteristics of thrombin and its receptor, and the role of Ca2+, PKC, Rho GTPases families, tyrosine kinase/phosphatase pathway, combined with the function of S1P and autophagy-related pathways.

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