Adipose-derived stem cell exosomes attenuates myofibroblast transformation via inhibiting autophagy through TGF-β/Smad2 axis in oral submucosal fibrosis.
Xu J., Wang Y., Shao Z., Zhou Y., Bin X., Liu L.
Animal Study, published in J Nanobiotechnology (2024) — 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
- J Nanobiotechnology (2024)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 39702233
- PMCID
- PMC11658435
- DOI
- 10.1186/s12951-024-03067-2
- Citations
- 5
Abstract (original English)
Oral submucous fibrosis (OSF) is a precancerous condition that poses substantial health risks. OSF is mainly caused by betel nut chewing behavior, but its pathogenesis is still unclear and there is no effective treatment strategy. The transformation of fibroblasts to myofibroblast is the key pathological change in the development of OSF. We isolated fibroblasts from human oral mucosa and induced them into myofibroblasts by arecoline, during which autophagy was significantly activated. Here, we found that adipose-derived stem cell exosomes (ADSCs-EXO) could inhibit autophagy to regulate myofibroblast phenotype, and transcriptome sequencing analysis suggested that this process is closely related to the TGF-β pathway. The interplay between autophagy and TGF-β pathway was examined through modulation the two with autophagy activators and inhibitors, TGF-β receptor activators and inhibitors. Results showed that in vitro, the TGF-β/Smad2 pathway augmented autophagy and promoted myofibroblast transformation. The transcriptome information of ADSCs-EXO showed that it contains a large number of miRNAs. Among them, miR-125a-5p could target Smad2. In vivo, injection of ADSCs-EXO alleviated OSF in mice, during which TGF-β and autophagy signals were inhibited. We suggested that ADSCs-EXO could inhibit myofibroblast transformation via inhibiting autophagy through TGF-β/Smad2 axis in OSF, provi
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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