[关键词]
[摘要]
视神经脊髓炎谱系疾病(NMOSD)是一种以中枢神经系统炎症和脱髓鞘为主要特征的自身免疫性疾病，其发病机制尚未完全阐明。最新研究表明，核因子-κB(NF-κB)信号通路在 NMOSD 的病理生理过程中发挥着关键作用。NF-κB 通路的异常激活可导致视网膜神经节细胞(RGCs)、免疫细胞、神经胶质细胞及血-脑屏障内皮细胞等多种细胞类型的活化，继而诱发促炎因子的释放，导致髓鞘损伤，最终参与 NMOSD 的发生与进展。NF-κB 信号通路抑制剂能够特异性地抑制促炎细胞因子的表达，调节异常免疫反应，展现出作为治疗靶点的显著潜力。当前，NF-κB 信号通路在 NMOSD 中的深入研究不仅揭示了其复杂的发病机制，也为实现精准治疗提供了全新的理论依据与方向。未来研究可进一步开发细胞特异性 NF-κB 抑制剂以提升治疗精准性，同时结合纳米递药系统增强药物对血-脑屏障的穿透效率，并探索该通路相关生物标志物以推动临床分层与个体化治疗。
[Key word]
[Abstract]
Neuromyelitis optica spectrum disorder(NMOSD)is an autoimmune disorder characterized primarily by inflammatory demyelination of the central nervous system, the pathogenesis of which remains incompletely elucidated. Recent research has demonstrated that the nuclear factor-kappa B(NF-κB)signaling pathway plays a pivotal role in the pathophysiology of NMOSD. Aberrant activation of the NF-κB pathway can induce the activation of various cell types, including retinal ganglion cells(RGCs), immune cells, glial cells, and blood-brain barrier endothelial cells, subsequently inducing the release of pro-inflammatory cytokines, resulting in myelin damage, and ultimately contributing to the onset and progression of NMOSD. Inhibitors targeting the NF-κB signaling pathway can specifically downregulate the expression of pro-inflammatory cytokines and modulate immune responses, demonstrating substantial potential for clinical application as therapeutic targets. Current in-depth research on the NF-κB pathway in NMOSD not only reveals its complex pathogenic mechanisms, but also provides a new theoretical basis and direction for precision therapy. Future studies may focus on developing cell-specific NF-κB inhibitors to enhance therapeutic precision, combining nanodrug delivery systems to improve drug penetration across the blood-brain barrier, and exploring biomarkers related to this pathway to advance clinical stratification and personalized treatment.
[中图分类号]
[基金项目]
无锡市卫健委中青年拔尖人才资助计划(No.BJ2023036)
