Abstract: Spinal cord injury is a severe neurological condition characterized by the permanent loss of nerve cell function and a failure in neural circuit reconstruction—key factors contributing to disability. Therefore, exploring effective strategies to promote the repair and regeneration of nerve cells after spinal cord injury is crucial for optimizing patient prognosis. The purpose of this paper is to conduct an in-depth review of the pathological changes in nerve cells after spinal cord injury and to present the state of research on the role of exercise training in promoting the repair and regeneration of nerve cells after spinal cord injury. In terms of the intrinsic growth capacity of neurons, disruptions in the dynamic balance between growth cones and the cytoskeleton, the dysregulation of transcription factors, abnormal protein signaling transduction, and altered epigenetic modifications collectively hinder axonal regeneration. Additionally, the microenvironment of neurons undergoes a series of complex changes, initially manifesting as edema, which may be exacerbated by spinal cord ischemiareperfusion injury, further increasing the extent of nerve cell damage. The abnormal proliferation of astrocytes leads to the formation of glial scars, creating a physical barrier to nerve regeneration. The inflammatory response triggered by the excessive activation of microglia negatively impacts the process of nerve repair. Non-invasive interventions involving exercise training have shown significant potential in promoting nerve repair as part of a comprehensive treatment strategy for spinal cord injury. Specifically, exercise training can reshape the growth cone and cytoskeletal structures of neurons, regulate transcription factor activity, modulate protein signaling pathways, and influence epigenetic modifications, thereby activating the intrinsic repair mechanisms of neurons. Moreover, exercise training can regulate the activation state of astrocytes, optimize the inflammatory response and metabolic processes, promote astrocyte polarization, enhance angiogenesis, reduce glial scar formation, and modulate the expression levels of nerve growth factors. It also effectively helps regulate microglial activation, promotes axonal regeneration, and improves phagocytic function, thereby optimizing the microenvironment for nerve repair. In terms of clinical translation, we summarize the preliminary results of new drug research and development efforts, the development of innovative devices, and the use of exercise training in promoting clinical advancements in nerve repair following spinal cord injury, while considering their limitations and future application prospects. In summary, this review systematically analyzes findings relating to the pathological changes occurring in nerve cells after spinal cord injury and emphasizes the critical role of exercise training in facilitating the repair and regeneration of nerve cells. This work is expected to provide new ideas and methods for the rehabilitation of patients with spinal cord injury.

Key words: astrocytes, axons, edema, exercise, inflammation, microglia, nerve regeneration, neurons, oxidative stress, spinal cord injury