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.
