Accelerating Bone Healing With METTL3 Overexpressed Adipose-Derived Stem Cells in Osteoporotic Rats.

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)

The treatment of postmenopausal osteoporosis (OP) presents a multifaceted challenge. Nonetheless, emerging research indicates a significant association between the N6-methyladenosine (m6A) methylase METTL3 and osteogenesis in OP. To investigate Mettl3's impact on osteogenic potential and the underlying molecular mechanisms, an OP rat model was established via ovariectomy (OVX). Osteoporotic adipose-derived stem cells (OP-ASCs) were then isolated. Results indicated a significant downregulation of Mettl3 expression in OP-ASCs. Subsequently, OP-ASCs were transfected with overexpressed Mettl3 lentivirus and treated for Dickkopf-related protein-1 (DKK1). Overexpression of the Mettl3 gene led to increased levels of osteogenic factors. DKK1 attenuated osteoblastic differentiation capacity in the Mettl3 overexpression group by inhibiting the Wnt signalling pathway. Consistent results were observed in vivo experiments. In conclusion, overexpression of Mettl3 promotes osteogenesis in OP-ASCs by activating the Wnt/β-catenin pathway.

Evidence level

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

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