Komarova Yulia A, Kruse Kevin, Mehta Dolly, Malik Asrar B
From the Department of Pharmacology and the Center for Lung and Vascular Biology, University of Illinois College of Medicine, Chicago.
Circ Res. 2017 Jan 6;120(1):179-206. doi: 10.1161/CIRCRESAHA.116.306534.
The monolayer of endothelial cells lining the vessel wall forms a semipermeable barrier (in all tissue except the relatively impermeable blood-brain and inner retinal barriers) that regulates tissue-fluid homeostasis, transport of nutrients, and migration of blood cells across the barrier. Permeability of the endothelial barrier is primarily regulated by a protein complex called adherens junctions. Adherens junctions are not static structures; they are continuously remodeled in response to mechanical and chemical cues in both physiological and pathological settings. Here, we discuss recent insights into the post-translational modifications of junctional proteins and signaling pathways regulating plasticity of adherens junctions and endothelial permeability. We also discuss in the context of what is already known and newly defined signaling pathways that mediate endothelial barrier leakiness (hyperpermeability) that are important in the pathogenesis of cardiovascular and lung diseases and vascular inflammation.
血管壁内衬的单层内皮细胞形成了一个半透屏障（除相对不透性的血脑屏障和视网膜内屏障外的所有组织中），该屏障调节组织液稳态、营养物质运输以及血细胞跨屏障迁移。内皮屏障的通透性主要由一种称为黏附连接的蛋白质复合物调节。黏附连接不是静态结构；它们会在生理和病理环境中响应机械和化学信号而持续重塑。在这里，我们讨论对连接蛋白翻译后修饰以及调节黏附连接可塑性和内皮通透性的信号通路的最新见解。我们还结合已知和新定义的介导内皮屏障渗漏（高通透性）的信号通路进行讨论，这些信号通路在心血管和肺部疾病以及血管炎症的发病机制中很重要。
