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.

中文翻译：

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神经突修复的机制。

收到损伤信号后，神经元可以激活各种途径来减少伤害，启动神经保护作用并修复受损的神经突而不会导致细胞死亡。在这里，我们回顾了神经突修复研究的最新进展，重点是神经元细胞自治机制，包括离子通道的新发现，这些离子通道可作为启动神经突修复和内在信号传导途径的关键调控因子以及促进神经突修复的转录和转录后因子。我们还涉及到有关树突切开后如何影响树突状细胞以及如何使受伤的神经突中的再生潜力最大化的报道。