GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE339nnn/GSE339142/primary200OKTranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE339142GEOGSEfalseFibronectin inhibition restores myelination in endothelial TNFR2-depedent non-remitting Experimental Autoimmune Encephalomyelitis [snRNA-Seq]Multiple Sclerosis (MS) is characterized by impaired remyelination and progressive neurodegeneration. We investigated the mechanisms underlying remyelination failure in Experimental Autoimmune Encephalomyelitis (EAE), a murine model of MS. TNFR2 deletion induces a severe non-remitting disease course and the main aim was to identify the cell population that drives this phenomenon. Through the analysis of single-nucleus RNA sequencing datasets, we identified endothelial cell-specific TNFR2 ablation as a driver of impaired remyelination. This effect was associated with fibronectin overexpression and accumulation in demyelinating lesions, highlighting the critical role of endothelial-specific TNFR2 signaling in central nervous system repair.2026/09/07GSE339142GSM9889062GSM9889061GSM9889060GSM9889063GSM9889059GSM988905828457339142Mus musculus