Division of Life Science, Molecular Neuroscience Center and State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, PR China.
Int Rev Neurobiol. 2012;105:91-115. doi: 10.1016/B978-0-12-398309-1.00006-8.
Injury to the central nervous system often leads to irreversible deficits because of the failure of damaged axons to regrow and restore the functional neural circuitry. Coordinated orchestration of multiple cellular processes including cytoskeletal dynamics and gene expression are essential for both developmental and regenerative axon growth. Recently, mounting evidence suggests that cyclin-dependent kinase 5 (Cdk5), a neuronal kinase implicated in almost all aspects of brain development and function, regulates multiple players required for axon formation and regeneration. Indeed, Cdk5 functions as a "plastic" kinase that maintains the axon growth ability by enabling efficient cytoskeletal reorganization, enhancing protein translation, reducing protein degradation, and promoting injury-induced gene transcription. Here, we summarize the up-to-date information on the mechanisms underlying the axon growth and regeneration after injury.
中枢神经系统损伤常常导致不可逆转的缺陷,因为受损的轴突无法再生并恢复功能神经回路。细胞过程的协调协调,包括细胞骨架动力学和基因表达,对于发育和再生轴突生长都是必不可少的。最近的证据表明,周期蛋白依赖性激酶 5(Cdk5)是一种在大脑发育和功能的几乎所有方面都有牵连的神经元激酶,它调节轴突形成和再生所需的多种因子。事实上,Cdk5 作为一种“可塑性”激酶,通过使细胞骨架重组更有效、增强蛋白质翻译、减少蛋白质降解和促进损伤诱导的基因转录,维持着轴突生长的能力。在这里,我们总结了损伤后轴突生长和再生的最新机制信息。