DNA Methylation Drives Osteochondrogenic Reprogramming in Keloid Pathogenesis And Reveals Therapeutic Potential of Decitabine
M. Supp, PhD1,2; Caitlin Phillips, BS2; Jane Young, BS2; Jennifer M. Hahn, BS1; Heather M. Powell, PhD3,2; Sara Higginson, MD, FACS2
BACKGROUND
Keloids are fibroproliferative disorders characterized by excessive extracellular matrix deposition, high recurrence, and aberrant osteochondrogenic differentiation. Although epigenetic dysregulation has been implicated in keloid pathogenesis, whether genome- wide DNA methylation drives pathological cellular reprogramming remains unclear.
CONCLUSION
Our findings identify DNA methylation as a central driver of aberrant osteochondrogenic reprogramming in keloid fibrosis and demonstrate that this pathological cell-fate program is therapeutically reversible. These results position keloids as a model of epigenetically driven fibrotic disease and support DNA methylation-targeted therapy as a rational strategy for preventing fibrosis progression and recurrence.
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