Different from neurons in the peripheral nervous system, mature neurons in the mammalian central nervous system often fail to regenerate after injury. Recent studies have found that calcium transduction, injury signaling, mitochondrial transportation, cytoskeletal remodeling and protein synthesis play essential roles in axon regeneration. Firstly, axon injury increases the intracellular concentration of calcium, and initiates the injury signaling pathways including cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) and dual leucine kinase (DLK), which are found to promote axon regeneration in multiple animal injury models. The second step for axonal regrowth is to rebuild growth cones. Overexpressing proteins that promote dynamics of microtubules and actin filaments is beneficial for the reassembly of cytoskeletons and initiation of new growth cones. Thirdly, mitochondria, the power factory for cells, also play important roles in growth cone formation and axonal extension. The last but not the least important step is the regulation of gene transcription and protein translation to sustain the regrowth of axons. This review summarizes important findings revealing the functions and mechanisms of these biological progresses.
与外周神经系统的神经元不同，中枢神经系统中成熟的神经元往往无法实现损伤后再生。近期，有研究发现钙离子传导损伤信号、线粒体运输、细胞骨架重构和蛋白质合成在轴突再生中发挥重要的功能。神经元损伤发生后，细胞内钙离子浓度升高，通过钙离子介导的环腺苷酸（cAMP）-蛋白激酶A（PKA）信号通路活化可激活下游双亮氨酸激酶（DLK），在多种动物损伤模型中促进轴突再生。轴突再生需要生长锥的重构，这一进程需要细胞骨架的有序组装，在损伤处表达特定促进微管和微丝聚合的基因可有效促进生长锥的重构。此外，负责供能的线粒体也会影响生长锥的重构和轴突再生能力。最后，研究还发现多个调控基因表达与蛋白合成的通路可促进轴突再生。本综述将重点概括这些对轴突再生有重要作用的生理过程和分子机制。
Keywords: Axon; Mitochondrial transportation; Model organisms; Regeneration; Review.