METTL3 mediated m6A methylation to promote mandibular condyle fracture healing via TGFB/Smad signaling pathway
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 TGFB/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.