ArticleInternational journal of molecular medicine2026
Oxygen‑sensing histone demethylase KDM6A modulates chondrocyte‑to‑osteoblast transdifferentiation by activating the Wnt/β‑catenin pathway.
Article in International journal of molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Immunometabolic reprogramming in osteoporosis-osteoarthritis comorbidity: from inflammaging to osteochondral unit degeneration.Frontiers in immunology · 2026Review
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11 authors.
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Abstract
Fracture healing is a complex biological process involving chondrocyte (CH) differentiation and endochondral ossification. A subset of CHs may transdifferentiate into osteoblasts, enhancing bone regeneration. The oxygen‑sensing histone demethylase lysine demethylase 6A (KDM6A) and local oxygen microenvironment are hypothesized to serve pivotal roles in modulating this transition; however, the precise regulatory mechanisms remain unclear. To assess the role of KDM6A, an oxygen‑sensitive histone demethylase, in endochondral ossification, an inducible cartilage‑specific Kdm6a‑knockout mouse model was generated. Single‑cell RNA sequencing (scRNA‑seq) analysis was performed in a mouse tibial fracture model to characterize CH subpopulations and their fate transitions during bone repair. scRNA‑seq identified distinct CH subpopulations, including chondrocyte‑derived osteoprogenitors (CDOPs), which acted as osteoblast precursors during endochondral ossification. Pseudotime trajectory analysis revealed a bifurcated differentiation pathway, with CDOPs exhibiting rapid osteoblast conversion. Functional enrichment analyses implicated the Wnt/β‑catenin pathway in this transition. In vitro, CHs isolated from bone callus of KDM6A‑knockout and control mice were induced to undergo transdifferentiation into osteoblasts under varying oxygen tensions. The expression levels of chondrogenic markers, osteogenic differentiation‑related indicators and canonical Wnt signaling molecules, as well as the levels of histone dimethylation of H3K27 (H3K27me2) and trimethylation of H3K27 (H3K27me3) at their promoter regions, were assessed. In vivo, the molecular and functional consequences of KDM6A deficiency were characterized through histopathological evaluation and bone microarchitecture analysis.
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