Oxygen‑sensing histone demethylase KDM6A modulates chondrocyte‑to‑osteoblast transdifferentiation by activating the Wnt/β‑catenin pathway

, KDM6A‑knockout mice exhibited osteogenic defects and delayed fracture healing compared with control mice. KDM6A serves as a pivotal oxygen sensor that drives CH‑to‑osteoblast transdifferentiation and enhances fracture healing through Wnt/β‑catenin pathway activation. The KDM6A‑mediated oxygen response mechanism is a potential target for enhancing bone regeneration during fracture repair.