ArticleScientific reports2026
METTL3-mediated m6A methylation to promote mandibular condyle fracture repair via TGF-β/Smad signaling pathway.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Mandibular condylar fractures are common maxillofacial injuries. N6-methyladenosine (m6A), one of the most abundant eukaryotic mRNA modifications, has not yet been clearly elucidated in terms of its specific role in condylar fracture repair. A mandibular condyle fracture rat model was established. Micro-CT scans and biochemical indicators were measured at 1- and 5 weeks post-fracture. The expression levels of m6A methylation-related enzymes were analyzed. METTL3 knockdown and overexpression models were constructed to evaluate structural healing via micro-CT, biomechanical properties, osteogenesis/chondrogenesis-related proteins, and the TGF-β/Smad signaling pathway. BMSCs were isolated for in vitro analyses, including cell viability, apoptosis, osteogenic differentiation, signaling pathway protein expression, and MeRIP-seq analysis. MeRIP-qPCR, RNA pull-down, and mRNA stability assays were used to verify METTL3-mediated m6A methylation targets. Compared to the 1-week group, the biochemical indicators in the 5-week group significantly increased, accompanied by upregulated METTL3 and downregulated FTO expression. METTL3 knockdown delayed fracture repair, disrupted bone structure, reduced osteogenic markers, and enhanced chondrogenic differentiation. Conversely, METTL3 overexpression significantly promoted bone healing and osteogenic differentiation. In vitro, METTL3 silencing reduced BMSC viability and inhibited osteogenic potential, along with suppression of TGF-β/Smad and RhoA/BMP9 signaling pathways. MeRIP-seq revealed extensive changes in m6A methylation peaks after METTL3 knockdown, identifying IGF-BP3 as a key target. MeRIP and RNA pull-down assays confirmed IGF-BP3 as a METTL3-mediated m6A modification target. METTL3 enhances IGF-BP3 mRNA stability through m6A methylation, subsequently activating the TGF-β/Smad signaling pathway to promote BMSC osteogenic differentiation and condylar fracture repair. This study highlights the critical role of METTL3-mediated m6A modification in mandibular condyle fracture repair and provides potential molecular targets for bone tissue engineering and clinical intervention.
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