To investigate the role of Wnt7a in corneal epithelial repair and its underlying mechanisms.Immunohistochemistry and immunofluorescence were used to assess Wnt7a expression in mouse corneas under normal and injury conditions. Human corneal epithelial cells (HCECs) were treated with Wnt7a siRNA or recombinant human Wnt7a (rhWnt7a) to evaluate proliferation (CCK-8 assay) and migration (scratch assay). Transcriptome sequencing and western blotting were performed to identify Wnt7a-regulated pathways and proteins.Under normal conditions, Wnt7a was predominantly localized to the corneal limbus basal cells. Following corneal injury, its expression significantly increased in central corneal epithelial cells and co-localized with nuclei during repair. Wnt7a siRNA suppressed HCEC proliferation and migration, while rhWnt7a enhanced proliferation. Transcriptome analysis revealed upregulation of cell adhesion-related genes (e.g., FN1, ITGBs, LAMs), particularly fibronectin (FN), validated by increased FN protein levels after rhWnt7a treatment. Pathway enrichment implicated PI3K/Akt, Wnt signaling, and ECM-receptor interactions.Wnt7a promotes corneal epithelial repair by enhancing migration and proliferation, primarily through upregulating fibronectin and ECM-related pathways. These findings highlight Wnt7a as a potential therapeutic target for accelerating corneal wound healing.© 2025. The Author(s), under exclusive licence to Springer Nature B.V.