Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

Extracellular vesicles from adipose-derived mesenchymal stem cells prevent high glucose-induced retinal ganglion cell pyroptosis through a microRNA-26a-5p-dependent mechanism.

Tang L., Zhang J., Gao J.

Animal Study, published in J Diabetes Investig (2025) — 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 Diabetes Investig (2025)
Country
Japan
Reported sample size
—
Source database
PubMed
PMID
40569812
PMCID
PMC12400376
DOI
10.1111/jdi.70100
Citations
3

Abstract (original English)

Objective Mesenchymal stromal/stem cells have neuroprotective effects that limit damage to the retina, which is predominantly mediated by the released extracellular vesicles (EVs). This study aims to investigate the protective effect of adipose-derived mesenchymal stem cell-derived EVs (ADSC-EVs) against pyroptosis of retinal ganglion cells (RGCs). Methods ADSC-EVs were isolated and then characterized. Mouse primary RGCs exposed to high glucose (HG) were applied for in vitro experiments. miR-26a-5p expression in RGCs after ADSC-EV treatment was determined by RT-qPCR. Target relation between miR-26a-5p and histone deacetylase 4 (HDAC4) was identified by luciferase reporter assay. miR-26a-5p blockad and HDAC4 ectopic expression experiments were conducted to clarify their functions in the pyroptosis of RGCs. The pyroptosis-associated protein GSDMD-N, inflammatory factors, and cell death were further evaluated by western blot, ELISA, and LDH assays, respectively. Results Exposure to HG reduced RGC viability and increased cell death, GSDMD-N protein level, and IL-1β and IL-18 levels, indicating pyroptosis induction. However, these HG-caused alterations could be reversed by ADSC-EVs. ADSC-EVs transferred miR-26a-5p into RGCs where miR-26a-5p targeted HDAC4 to limit its expression and enhance histone H3 lysine 27 acetylation (H3K27ac) modification at the nuclear factor erythroid 2-rel

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
MicroRNAsPyroptosisAnimalsRetinal Ganglion CellsMesenchymal Stem CellsMiceExtracellular VesiclesGlucoseHistone DeacetylasesMice, Inbred C57BL

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