Spinal cord injury (SCI) is a severe trauma to the central nervous system, and secondary injury-induced progressive neuronal loss plays a critical role in the development of neurological dysfunction. The molecular mechanisms underlying ferroptosis are intricately linked to dysregulation in iron metabolism, lipid metabolism, and amino acid homeostasis, all of which are implicated in the pathophysiology of SCI. This article provides a systematic review of the molecular mechanisms of ferroptosis and its regulatory influence on the pathological progression of spinal cord injury. Furthermore, it summarizes current therapeutic strategies targeting key pathways involved in ferroptosis, including restoration of iron homeostasis, inhibition of lipid peroxidation, and correction of amino acid metabolic imbalances. Recent advances in traditional Chinese medicine, stem cell-derived exosome therapy, and microRNA-based interventions are also discussed, aiming to provide a theoretical foundation for future ferroptosis-targeted approaches in spinal cord injury repair.