ADSC-derived exosomes inhibit myofibroblast transdifferentiation and attenuate airway stenosis via METTL3-mediated m6A modification of TLR2.
Zhang G., Zheng T., Guo W., Zhuang X.
Animal Study, published in Am J Transl Res (2026) — summary generated from the PubMed abstract.
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
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Am J Transl Res (2026)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41676287
- PMCID
- PMC12886091
- DOI
- 10.62347/XPQC7344
Abstract (original English)
Objective To 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. Methods ADSC-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. Results ADSC-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. Conclusion ADSC-Exos promote airway repair by upregulating METTL3, which enhances m6A methylation of TLR2 mRNA, do
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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