Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Adipose-derived mesenchymal stem cell-derived extracellular vesicles carry microRNA-214-3p to target GSTZ1 to curb ferroptosis in lung epithelial cells during sepsis.

Li M., Zhong J., Li X.

Animal Study on Hip, published in Cytotechnology (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
Cytotechnology (2025)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
40611882
DOI
10.1007/s10616-025-00793-9
Citations
1

Abstract (original English)

Ferroptosis pitches in sepsis-caused pulmonary diseases. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) pitches in ferroptosis. This study explored the mechanism of adipose-derived MSC-EVs (ADMSC-EVs) protecting against ferroptosis in lung epithelial cells during sepsis. ADMSC-EVs were extracted using ultracentrifugation, followed by ADMSC and EV characterization. MLE-12 cells received 24-h lipopolysaccharide (LPS) treatment to mimic sepsis-induced ferroptosis, and treatment with EVs, a ferroptosis inhibitor (Fer-1), or the glutathione S-transferase zeta 1 overexpression plasmid. Cell viability, and levels of glutathione (GSH), malondialdehyde (MDA), Fe 2+ , reactive oxygen species (ROS), lipid peroxidation (LPO), ferroptosis-related proteins (glutathione peroxidase 4 [GPX4], solute carrier family 7 member 11 [SLC7A11]), miR-214-3p, and GSTZ1 were assessed. A mouse model of sepsis-induced acute lung injury was established by cecal ligation and puncture, and mice were intratracheally injected with EVs, followed by evaluation of resting ventilation per minute, inspiratory resistance, dynamic lung compliance, lung wet-to-dry weight ratio, and lung tissue cell morphology. The miR-214-3p-GSTZ1 targeted relationship was analyzed by Starbase database and dual-luciferase assay. LPS treatment reduced MLE12 cell viability, decreased GSH, GPX4 and SLC7A11 levels, and eleva

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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