Howard Hughes Medical Institute, Department of Physiology, University of California, San Francisco, CA 94158, USA.
Howard Hughes Medical Institute, Department of Physiology, University of California, San Francisco, CA 94158, USA.
Curr Opin Neurobiol. 2020 Aug;63:53-58. doi: 10.1016/j.conb.2020.02.010. Epub 2020 Apr 8.
Upon receiving injury signals, neurons can activate various pathways to reduce harm, initiate neuroprotection, and repair damaged neurite without cell death. Here, we review recent progresses in the study of neurite repair focusing on neuronal cell-autonomous mechanisms, including new findings on ion channels that serve as key regulators to initiate neurite repair and intrinsic signaling pathways and transcriptional and post-transcriptional factors that facilitate neurite repair. We also touch upon reports on how dendrites may be affected upon axotomy and how the regeneration potential in injured neurites might be maximized.
神经元在接收到损伤信号后,可以激活多种途径来减轻伤害、启动神经保护并修复受损的轴突而不导致细胞死亡。在这里,我们综述了轴突修复的研究进展,重点关注神经元自主机制,包括离子通道作为启动轴突修复的关键调节剂的新发现,以及促进轴突修复的内在信号通路和转录后因子。我们还提到了关于轴突切断后树突如何受到影响以及如何最大限度地提高损伤轴突的再生潜力的报告。