Research findings indicate that programmed cell death (PCD) plays a pivotal role in the pathophysiology of spinal cord injury (SCI), and a recently discovered form of cell death, disulfidptosis, has emerged as a novel phenomenon. However, the characterization of disulfidptosis-related genes in SCI remains insufficiently explored. We retrieved SCI-related data from the Gene Expression Omnibus (GEO) database and identified three key genes associated with disulfidptosis in human SCI (CAPZB, SLC3A2, and TLN1), whose mediated signaling pathways are closely intertwined with SCI. Subsequent functional enrichment analysis suggested that these genes may regulate multiple pathways and exert corresponding roles in SCI pathology. Moreover, we predicted potential targeted drugs for the key genes along with their transcription factors and constructed an intricate regulatory network. CIBERSORT analysis revealed that CAPZB, SLC3A2, and TLN1 might be implicated in modulating changes within the immune microenvironment of individuals with SCI. Our study provides compelling evidence confirming the significant involvement of disulfidptosis following SCI while offering valuable insights into its underlying pathological mechanisms.