Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

ADSC-Exo-bFGF promotes skin wound healing and correlates with the PI3K/AKT signaling pathway activation.

Cheng S., Gong F., Ma G., Wang Y., Zhang P., Liu X.

Animal Study on Chronic Wound, Chronic Inflammation, published in J Mol Histol (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
J Mol Histol (2026)
Country
Netherlands
Reported sample size
—
Source database
PubMed
PMID
42461467
DOI
10.1007/s10735-026-10885-1

Abstract (original English)

Wound healing is a complex physiological process involving a variety of tissue repair cells. Adipose-derived stem cell (ADSC)-derived exosomes have demonstrated potential in promoting wound healing. Basic fibroblast growth factor (bFGF) is known to facilitate tissue regeneration. Nevertheless, the biological functions and detailed mechanisms of ADSC-Exo-bFGF in cutaneous wound healing remain largely unelucidated. The study aimed to construct a bFGF-glycosylphosphatidylinositol (GPI)-anchored exosome system (ADSC-Exo-bFGF) and further explore its therapeutic efficacy and underlying molecular mechanisms in skin wound healing. A eukaryotic expression plasmid carrying bFGF-GPI fusion gene was constructed and transfected into ADSCs. Secreted exosomes were isolated and characterized by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and western blotting. Hematoxylin and Eosin (H&E) staining and Masson's trichrome staining were used for histological assessment. Inflammatory cytokines in wound tissues and cell supernatants were quantified by enzyme-linked immunosorbent assay (ELISA). Cell viability was evaluated by Cell Counting Kit-8 (CCK-8) assay. Scratch assay was applied for determining cell migration ability. The protein levels of bFGF and the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway related proteins were assessed using wester

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.

How we grade evidence
Wound HealingProto-Oncogene Proteins c-aktAnimalsSignal TransductionFibroblast Growth Factor 2ExosomesPhosphatidylinositol 3-KinasesSkinMiceHumans

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