GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE327nnn/GSE327158/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327158GEOGSEfalseA novel ocular fibrosis signature for AMD using transcriptomic profiling of the two-stage laser-induced subretinal fibrosis mouse model.Subretinal fibrosis is a major cause of irreversible vision loss in neovascular age-related macular degeneration (nAMD), yet conserved molecular signatures remain to be fully elucidated. Using RNA-seq on RPE/Choroid from a two-stage laser-induced subretinal fibrosis mouse model, we identified a novel core ocular fibrosis signature of 88 persistently upregulated genes across acute-to-chronic phases (days 3–10 post-injury). This signature, enriched in epithelial-mesenchymal transition, complement activation, and inflammatory pathways, showed choroid-specific expression with minimal retinal involvement. Cross-validation in independent chronic mouse data and multiple human AMD datasets (peripheral retina, surgically extracted CNV membranes, and macular RPE/choroid) confirmed progressive enrichment in advanced disease stages. Immunofluorescence in human fibrotic tissue validated key genes (Tenascin C, Tissue Inhibitor of Metalloproteinases-1, and Apelin receptor) with co-localization to myofibroblast-like cells and microglia. This persistent, cross-species-validated signature potentially highlights conserved fibrogenic drivers and offers a translational tool for biomarker development and targeted antifibrotic therapies in nAMD.2026/08/26GSE327158GSM9650132GSM9650121GSM9650120GSM9650131GSM9650130GSM9650136GSM9650125GSM9650114GSM9650135GSM9650124GSM9650113GSM9650123GSM9650134GSM9650133GSM9650122GSM9650129GSM9650118GSM9650128GSM9650117GSM9650127GSM9650116GSM9650126GSM9650115GSM965011930172327158Mus musculus[42615798]