脊髓损伤导致脊髓损伤灶平面以下的感觉运动功能障碍及自主神经功能障碍，造成持久性功能 损伤。功能恢复需要完整神经元的代偿性轴突发芽或受损轴突的再生，而神经元轴突再生能力的激活 受到转录调控变化的限制。表观遗传学是启动和维持再生转录反应的关键因素，其中组蛋白共价修饰 可调控神经损伤后染色质结构的变化，进而影响转录输出，为促进脊髓损伤后轴突再生的研究提供了新 靶点。本文就组蛋白共价修饰对脊髓损伤后轴突再生相关的表观调控机制进行综述，为临床上脊髓损 伤修复提供新的治疗思路。

Spinal cord injury (SCI) elicits sensory, motor, and autonomic dysfunctions caudal to the lesion site, resulting in enduring functional deficits. Successful recovery hinges upon compensatory axonal sprouting from intact neurons or regeneration of damaged axons, a process constrained by transcriptional regulatory dynamics. Epigenetics emerges as a pivotal determinant in instigating and sustaining regenerative transcriptional cascades. Specifically, histone covalent modifications intricately modulate post-injury chromatin restructuring, consequently influencing transcriptional dynamics. This review delineates the epigenetic regulatory framework governing post-SCI axonal regeneration, emphasizing the role of histone covalent modifications as potential therapeutic targets to enhance clinical interventions for SCI repair.