VEGFR2 介导的血管通透性
中文名称
通路描述
由内皮一氧化氮合酶（eNOS）产生的自由基一氧化氮（NO）是正常血管生物学和病理生理学中重要的血管活性物质。它在血管功能中发挥重要作用，如血管舒张和血管生成（Murohara 等。1998, Ziche 等。1997）。据报道，NO 是 VEGF 介导的血管生成反应的下游介质，但 NO 促进新血管形成的机制尚不清楚（Babaei & Stewart 2002）。在血管生成的早期步骤中，观察到持续血管舒张和血管通透性增加，表明这些血流动力学变化在血管生成过程中是不可或缺的。VEGF 诱导的 NO 产生可以通过 PI3K 激活或 PLC-gamma 依赖的方式发生。一旦两条途径都激活，它们都汇聚到 AKT 磷酸化 eNOS，释放 NO（Lin & Sessa 2006）。VEGF 还通过 VEGFR-2-Src-Vav2-Rac-PAK 信号轴促进 VE-cadherin 的内吞作用来调节血管通透性。
英文描述
VEGFR2 mediated vascular permeability The free radical nitric oxide (NO), produced by endothelial NO synthase (eNOS), is an important vasoactive substance in normal vascular biology and pathophysiology. It plays an important role in vascular functions such as vascular dilation and angiogenesis (Murohara et al. 1998, Ziche at al. 1997). NO has been reported to be a downstream mediator in the angiogenic response mediated by VEGF, but the mechanism by which NO promotes neovessel formation is not clear (Babaei & Stewart 2002). Persistent vasodilation and increase in vascular permeability in the existing vasculature is observed during the early steps of angiogenesis, suggesting that these hemodynamic changes are indispensable during an angiogenic processes. NO production by VEGF can occur either through the activation of PI3K or through a PLC-gamma dependent manner. Once activated both pathways converge on AKT phosphorylation of eNOS, releasing NO (Lin & Sessa 2006). VEGF also regulates vascular permeability by promoting VE-cadherin endocytosis at the cell surface through a VEGFR-2-Src-Vav2-Rac-PAK signalling axis.
所含基因
27 个基因