RAGE/NF-κB信号通路调控自噬对外周神经损伤修复影响的机制研究

Peripheral nerve injury is very common in clinic with poor recoery of neurological function. Our previous study indicates that pharmacological inhibition of mTOR signal to activate autophagy promotes peripheral nerve regeneration and motor recovery following sciatic nerve crush injury in rats【J Mol Neurosci, 2016】. Researches have shown that RAGE regulates autophagy via NF-κB sinal. Therefore, we hypothesize that RAGE/NF-κB signal regulates autophagy that effects recovery of Peripheral nerve injury. The project is based on our previous study and further explore the molecular mechanism of RAGE/NF-κB signal regulating autophagy which effects the recovery in Peripheral nerve injury, so as to seek new targets for the clinical treatment of peripheral neuropathy.

外周神经损伤在临床上极为常见，修复后神经功能的恢复欠佳。我们的前期研究表明，通过拮抗mTOR激活自噬可促进外周神经损伤神经再生与运动功能的恢复【J Mol Neurosci, 2016】。有研究表明，高级糖化蛋白终端产物受体（RAGE）通过NF-κB信号调控自噬。据此我们提出假设： RAGE/NF-κB信号通路调控自噬，影响外周神经损伤修复。本项目在前期的研究基础上，深入探讨RAGE/NF-κB信号通路调控自噬，从而影响外周神经损伤修复的分子机制，为临床治疗外周神经病变寻找新的靶点。