Adipose-derived mesenchymal stem cell exosomes ameliorate copper metabolism dysregulation and reduce cuproptosis caused by liver IRI.
Cao L., Li P., Ma Y., Lu X., Wang Y., Wang H.
Laboratory Study, published in Front Vet Sci (2026) — 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
- Laboratory Study
- Journal
- Front Vet Sci (2026)
- Country
- Switzerland
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42528680
- DOI
- 10.3389/fvets.2026.1895340
Abstract (original English)
Hepatic ischemia reperfusion injury is an important pathological factor leading to complications after hepatectomy and transplantation. Although cuproptosis has been reported as a new paradigm of programmed death triggered by copper homeostasis imbalance, its regulatory mechanisms and intervention strategies in liver IRI remain to be fully elucidated. The purpose of this study was to reveal the role of cuproptosis in liver IRI, and to elucidate the molecular mechanism by which adipose-derived stem cell exosomes (ADSC-Exos) exert therapeutic effects by regulating copper metabolism. Rat IRI models were established to evaluate copper metabolism dysregulation and cuproptosis activation. Subsequently, miniature pig models underwent laparoscopic IRI induction to assess ADSC-Exos's effects on copper homeostasis restoration over 7 days post-injury. We found that liver IRI disrupts copper homeostasis through a dual pathway: it inhibits membrane transporters CTR1 and ATP7B to affect copper ion excretion, and down-regulates intracellular copper chaperones ATOX1, CCS and COX17 expression, resulting in intracellular copper metabolism disorders. Excessive copper ions will bind to the lipoylated protein DLAT, induce its oligomerization and mitochondrial Fe-S cluster protein depletion, eventually leading to cuproptosis in hepatocytes and aggravating IRI. The intervention of ADSC-Exos can effec
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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