The detail clinical information of 6 samples.

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.

研究结果显示，程序性细胞死亡（programmed cell death, PCD）在脊髓损伤（spinal cord injury, SCI）的病理生理过程中发挥关键作用，而新近发现的细胞死亡形式——二硫代死亡（disulfidptosis）已成为一项全新的研究现象。然而，目前针对脊髓损伤中二硫代死亡相关基因的特征解析仍有待深入探索。本研究从基因表达综合数据库（Gene Expression Omnibus, GEO）中获取脊髓损伤相关数据，鉴定出3个人类脊髓损伤中二硫代死亡相关的关键基因（CAPZB、SLC3A2及TLN1），这些基因介导的信号通路与脊髓损伤病理过程密切相关。后续的功能富集分析显示，上述基因可调控多条通路，并在脊髓损伤病理进程中发挥相应作用。此外，本研究还预测了上述关键基因的潜在靶向药物及其转录因子，并构建了复杂的调控网络。CIBERSORT分析结果显示，CAPZB、SLC3A2及TLN1可能参与调控脊髓损伤患者的免疫微环境变化。本研究提供了有力证据，证实二硫代死亡在脊髓损伤后发挥重要作用，并为其潜在病理机制提供了极具价值的研究视角。