Adipose mesenchymal stem cell-derived exosomes rescue mitochondrial function through SIRT1 to improve diabetic wound healing.
Bai X., Li Y., Wang P., Xu Z., Wei J., He T.
Animal Study on Diabetic Foot, Chronic Wound, Chronic Inflammation, published in Burns Trauma (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
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- Study type
- Animal Study
- Journal
- Burns Trauma (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41089383
- PMCID
- PMC12516946
- DOI
- 10.1093/burnst/tkaf017
- Citations
- 2
Abstract (original English)
Background Diabetic wounds represent the most common type of chronic wounds. Persistent inflammation and elevated oxidative stress are hallmark features of chronic wounds, where macrophage phenotypic polarization playing a critical role in the healing process. Adipose-derived mesenchymal stem cell exosomes (ADSC-exos) have shown promising therapeutic effects in the treatment of diabetic wounds by modulating macrophage function. This study aims to elucidate the specific downstream regulatory mechanisms through both in vitro and in vivo investigations. Methods A streptozotocin-induced diabetic mouse model and high glucose-stimulated RAW 264.7 macrophages were utilized to mimic diabetic microenvironments. Wound tissues were collected from patients with diabetic foot ulcer. A skin incision model was established in mice and ADSC-exos were given subcutaneously. Streptozotocin-induced diabetic myeloid-specific sirt1 -/- mice SIRT1 siRNA-transfected macrophages were employed to investigate the role of SIRT1 in vivo and in vitro . Wound healing rates were quantified. Mitochondrial function, lysosomal activity, autophagy flux, and inflammation status were systematically assessed. Results In diabetic mice and high glucose-treated macrophages, lysosomal dysfunction preceded mitochondrial and autophagy flux impairments. SIRT1 expression was significantly reduced in both diabetic wound tissu
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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