Level D· Preclinical EvidenceAnimal Study

Adipose mesenchymal stem cell-derived extracellular vesicles regulate PINK1/parkin-mediated mitophagy to repair high glucose-induced dermal fibroblast senescence and promote wound healing in rats with diabetic foot ulcer

Luo Y., Guo Q., Liu C., Zheng Y., Wang Y., Wang B.

Animal Study on Diabetic Foot, Chronic Wound, published in Acta Diabetol (2025) — summary generated from the PubMed abstract.

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
Acta Diabetol (2025)
Country
Germany
Reported sample size
PMID
39680129
DOI
10.1007/s00592-024-02422-x

Abstract (original English)

Diabetic foot ulcers (DFUs) cause prominent morbidity and mortality. Adipose mesenchymal stem cell (ASC)-derived extracellular vesicles (EVs) show property in facilitating diabetic wound healing, and we explored their role in DFU rats. ASCs were cultured in vitro, passaged and then identified by flow cytometry and induction of osteogenic/adipogenic differentiation. ASC-EVs were extracted and identified. DFU rat model was treated with ASC-EVs. High glucose (HG)-induced rat dermal fibroblasts were treated with ASC-EVs or 3-MA and sh-PINK1 plasmid in vitro. Wound healing was observed. Histological changes, inflammatory cytokines (TNF-α, IL-1β), and α-SMA and p21 double-positive cell level were assessed by HE staining, ELISA, and immunofluorescence. Mitochondrial membrane potential (MMP), cell viability and senescence, and ROS production in cells were assessed by fluorescence dye JC-1, CCK-8, SA-β-gal staining, and ROS kit. p21, LC3II/I, p62, PINK1 and parkin protein levels were determined by Western blot. DFU rats had slow wound healing and elevated levels of IL-1β, TNF-α, α-SMA and p21 double-positive cells, and SA-β-gal, while HG-induced cells had weakened viability, elevated ROS, SA-β-gal, p21 and p62 protein levels, and decreased LC3II/I, PINK1 and parkin protein levels and MMP, which were reversed by ASC-EVs. HG inhibited mitophagy by suppressing the PINK1/parkin pathway to a

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 comes from animal or laboratory studies and has not been confirmed in humans.

How we grade evidence
AnimalsWound HealingMitophagyRatsMesenchymal Stem CellsExtracellular VesiclesDiabetic FootUbiquitin-Protein LigasesCellular SenescenceFibroblasts

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