Met-Exo attenuates pyroptosis in miniature pig liver IRI by improving mitochondrial quality control.
Cao L., Li P., Liu T., Ma Y., Lu X., Wang H.
Animal Study, published in Int Immunopharmacol (2025) — summary generated from the PubMed abstract.
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
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
- Int Immunopharmacol (2025)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40068522
- DOI
- 10.1016/j.intimp.2025.114437
Abstract (original English)
Metformin(Met) and adipose-derived stem cell exosomes(ADSCs-Exo) both demonstrate therapeutic effects on mitochondrial dysfunction and pyroptosis. There is also a phenomenon of mutual promotion between these two pathological states. The synergistic effect of metformin-loaded exosomes (Met-Exo) via electroporation in a miniature pig liver ischemia-reperfusion injury (IRI) model remains unexplored. This study established a liver IRI model in miniature pigs to compare the effects of ADSCs-Exo and Met-Exo. We found that Met-Exo intervention better activated the Adenosine 5'-monophosphate activated protein kinase (AMPK)/NAD-dependent deacetylase sirtuin-1(SIRT1) axis, improved mitochondrial dynamics, promoted mitochondrial biogenesis, and inhibited the sustained excessive autophagy of mitochondria after liver IRI. It was then demonstrated that by improving mitochondrial dysfunction, ATP production in liver tissue could be ensured, and ROS generation could be suppressed. This also further inhibited the occurrence of pyroptosis and ensured that mitochondria were protected from gasdermin D-N(GSDMD-N) attack. Met-Exo inhibited the occurrence of pyroptosis through the above pathways, reducing the release of inflammatory factors such as IL-1β and IL-18, and alleviating inflammation. This provides a new therapeutic approach for clinical treatment of liver IRI and improving the success rate
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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