Demonstrates enhanced bone regeneration in craniofacial defects using HDAC4 inhibition, suggesting a new repair method.
Craniofacial large bone defects possess limited self-repair capacity. This study identifies histone deacetylase 4 (HDAC4) as a key epigenetic repressor of osteogenesis in human adipose-derived stem cells. Inhibiting HDAC4, either genetically or pharmacologically with tasquinimod, enhanced histone acetylation and activates SMAD4 expression, thereby promoting bone formation. A sustained-release hydrogel delivering tasquinimod was developed and demonstrated to significantly enhance bone regeneration in critical-sized cranial and mandibular defects in mice. The findings reveal a promising localized epigenetic strategy for repairing craniofacial bone defects.
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Yu et al. (2026) studied this question.
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