Adipose-derived stem cell exosomes alleviate TGF-β1-induced urethral stricture fibrosis by suppressing the TGF-β/Smad pathway and downstream PDGFR-β/RAS/ERK signaling.
Liang T., Deng C., Guo H., Dai Z., Jiang Y., Lu Y.
Animal Study, published in J Cell Commun Signal (2025) — 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 Cell Commun Signal (2025)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40520075
- PMCID
- PMC12162353
- DOI
- 10.1002/ccs3.70025
Abstract (original English)
This study aimed to investigate the therapeutic effects and underlying mechanisms of adipose-derived stem cell exosomes (ADSCs-exo) in ameliorating fibrosis in a rat model. ADSCs were isolated and cultured from rat adipose tissue, and ADSCs-exo were extracted via ultracentrifugation. Urethral fibrosis was induced by local injection of TGF-β1 (10 μg), followed by ADSCs-exo treatment. Urodynamic parameters were evaluated, and histological changes were evaluated using hematoxylin and eosin and Masson staining. Transcriptomic analysis and pathway enrichment were performed to identify signaling pathways regulated by ADSCs-exo. In vitro, urinary fibroblasts were stimulated with TGF-β1 and treated with ADSCs-exo alone or in combination with PDGF-BB (agonist) or imatinib (inhibitor). ADSCs-exo treatment significantly improved urodynamic function, reduced collagen deposition, and suppressed fibrosis-related protein expression in vivo. Transcriptomic analysis revealed platelet-derived growth factor and TGF-β pathways as major contributors to fibrosis. In vitro, ADSCs-exo significantly reduced TGF-β1-induced fibroblast proliferation, migration, and fibrosis-related protein expression, effects that were reversed by PDGF-BB and enhanced by imatinib. These findings were consistent in vivo, further supporting the hierarchical regulation of fibrosis-related signaling by ADSCs-exo. ADSCs-exo mi
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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