HDAC4 regulates hASC osteogenesis and bone regeneration by mediating SMAD4 via histone acetylation.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

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.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.