ArticleAmerican journal of translational research2026
ADSC-derived exosomes inhibit myofibroblast transdifferentiation and attenuate airway stenosis via METTL3-mediated m6A modification of TLR2.
Article in American journal of translational research, 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
objectiveTo investigate the therapeutic potential of adipose-derived stem cell exosomes (ADSC-Exos) in airway repair and the underlying mechanisms, with a particular focus on the role of N6-methyladenosine (m6A) modification.
methodsADSC-Exos were isolated and characterized via ultracentrifugation. In vitro effects of ADSC-Exos were evaluated using transforming growth factor-β1 (TGF-β1)-induced fibroblast models. A rabbit airway injury model was established, and exosomes were locally administered. Molecular mechanisms were investigated using methylated RNA immunoprecipitation sequencing (MeRIP-seq), RNA-seq, Western blotting, and qRT-PCR.
resultsADSC-Exos significantly upregulated the expression of m6A methyltransferase methyltransferase-like 3 (METTL3) in both in vivo and in vitro experiments. This upregulation further enhanced the m6A methylation level of Toll-like receptor 2 (TLR2) mRNA, leading to decreased TLR2 expression. Additionally, the phosphatidylinositol 3-kinase-protein kinase B (PI3K-AKT) signaling pathway was inhibited, accompanied by decreased expression of the myofibroblast markers α-smooth muscle actin (α-SMA) and Collagen I. Notably, overexpression of METTL3 reversed the inhibitory effects induced by ADSC-Exos on myofibroblast differentiation.
conclusionADSC-Exos promote airway repair by upregulating METTL3, which enhances m6A methylation of TLR2 mRNA, downregulates TLR2, and inhibits PI3K-AKT pathway activation, thereby inhibiting myofibroblast differentiation. This study reveals a novel epigenetic mechanism for the treatment of benign airway stenosis (BAS).
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