[关键词]
[摘要]
哺乳动物外周神经损伤后轴突能再生很长距离。在一定条件下，中枢神经系统受损后也能部分再生。Nogo是一种已经被证实的髓鞘相关抑制因子，中枢神经损伤后Nogo释放增加、表达增强，启动神经元凋亡过程，导致神经元死亡。我们从Nogo-A，Nogo-66，可溶性NgR片段、RhoA酶与Rho-A/Rho激酶信号通道、钙离子几个方面综述Nogo的作用机制，并探讨其在视神经损伤后神经再生中的应用前景。
[Key word]
[Abstract]
After mammalian peripheral nerve injury, axons can regenerate very long distance. In certain conditions, the central nervous system can also partially regenerate after damage. Nogo has been proved to be one of the myelin-associated inhibitors, after central nerve injury increased Nogo release, enhanced Nogo expression, start-up process of apoptosis, leading to neuronal death. In this paper, we summed up the mechanism of action of Nogo from Nogo-A, Nogo-66, soluble NgR fragments, RhoA enzyme and Rho-A/Rho kinase signaling pathway, calcium ion aspects, and discussed its application prospect in nerve regeneration after optic nerve injury.
[中图分类号]
[基金项目]
国家自然科学地区基金(No.31160206)
