Exosomal miR-4687-5p alleviates silica-induced fibrosis by inhibiting EMT via β-catenin targeting

Silicon dioxide (SiO₂) is a major occupational hazard causing irreversible pulmonary fibrosis. While epithelial-mesenchymal transition (EMT) is implicated in fibrosis, its regulation remains unclear. This study identified serum exosomal miR-4687-5p as significantly down-regulated in silicosis patients. Dual-luciferase assays confirmed β-catenin as its direct target. Using the exosome inhibitor GW4869, we demonstrated exosome-mediated transfer of miR-4687-5p from macrophages to lung epithelial cells. Treating epithelial cells with a miR-4687-5p mimic revealed its role in modulating EMT by inhibiting β-catenin nuclear translocation. Crucially, silencing β-catenin in murine lung tissue significantly attenuated silica-induced pulmonary fibrosis. Our findings establish that exosomal miR-4687-5p alleviates silicosis-related fibrosis by targeting β-catenin to suppress EMT, highlighting miR-4687-5p as a potential therapeutic target.