Endothelial tight junctions (TJs) regulate the transport of water, ions, and molecules through the paracellular pathway, serving as an important barrier in blood vessels and maintaining vascular homeostasis. In endothelial cells (ECs), TJs are highly dynamic structures that respond to multiple external stimuli and pathological conditions. Alterations in the expression, distribution, and structure of endothelial TJs may lead to many related vascular diseases and pathologies. In this review, we provide an overview of the assessment methods used to evaluate endothelial TJ barrier function both in vitro and in vivo and describe the composition of endothelial TJs in diverse vascular systems and ECs. More importantly, the direct phosphorylation and dephosphorylation of TJ proteins by intracellular kinases and phosphatases, as well as the signaling pathways involved in the regulation of TJs, including and the protein kinase C (PKC), PKA, PKG, Ras homolog gene family member A (RhoA), mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K)/Akt, and Wnt/β-catenin pathways, are discussed. With great advances in this area, targeting endothelial TJs may provide novel treatment for TJ-related vascular pathologies.

中文翻译：

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血管内稳态和疾病中的内皮紧密连接及其调节信号通路。

内皮紧密连接（TJs）调节水，离子和分子通过旁细胞途径的运输，是血管中的重要屏障并维持血管稳态。在内皮细胞（EC）中，TJ是高度动态的结构，可响应多种外部刺激和病理状况。内皮TJ的表达，分布和结构的改变可能导致许多相关的血管疾病和病理。在这篇综述中，我们提供了用于在体外和体内评估内皮TJ屏障功能的评估方法的概述，并描述了各种血管系统和EC中内皮TJ的组成。更重要的是，TJ蛋白被细胞内激酶和磷酸酶直接磷酸化和去磷酸化，以及涉及TJ调节的信号传导途径，包括蛋白激酶C（PKC），PKA，PKG，Ras同源基因家族成员A（RhoA），促分裂原激活蛋白激酶（MAPK），磷脂酰肌醇3激酶（PI3K）/ Akt和Wnt /β-catenin途径进行了讨论。随着这一领域的巨大进步，靶向内皮TJ可能为TJ相关血管病变提供新颖的治疗方法。