Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

FGF21-modified adipose stem cell-derived exosomes promote wound healing by activating fibroblast glycolysis through AMPK/mTOR signaling.

Chen K., Chen X., Wen C., Chen W., Liao Z., Chen Y.

Animal Study on Chronic Wound, published in Cell Signal (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

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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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
Cell Signal (2026)
Country
England
Reported sample size
—
Source database
PubMed
PMID
42551612
DOI
10.1016/j.cellsig.2026.112742

Abstract (original English)

Chronic wound healing disorders remain a significant clinical challenge, largely due to the limited effectiveness of conventional therapeutic strategies. Emerging evidence suggests that engineered exosomes represent a promising cell-free therapeutic approach. This study aimed to elucidate the mechanisms by which fibroblast growth factor 21 (FGF21)-modified adipose-derived mesenchymal stem cell (ADSC) exosomes promote wound healing. ADSCs overexpressing FGF21 were established using genetic engineering, and FGF21-enriched exosomes (Exo@FGF21) were isolated and characterized using transmission electron microscopy and nanoparticle tracking analysis. The biological effects of Exo@FGF21 on human skin fibroblasts (HSFs) were assessed through proliferation, migration, invasion, and apoptosis assays. Glycolytic activity, glucose consumption, lactate production, ATP levels, and hydroxyproline content were evaluated to investigate metabolic changes. Mechanistic studies involved pharmacological inhibition of AMPK and knockdown of PFKFB3. Therapeutic efficacy was further examined in a mouse full-thickness skin defect model. Exo@FGF21 exhibited typical exosomal morphology with diameters ranging from 80 to 150 nm and expressed canonical exosomal markers CD9 and CD63. In vitro, Exo@FGF21 significantly enhanced fibroblast proliferation, migration, and invasion, promoted collagen synthesis-relat

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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