Extracellular vesicles derived from hADSCs rescue acute pancreatitis by carrying p -STK3 to regulate Treg differentiation.
Xie R., Xiao G., Yang K., Wang X., Chen C., Zhou T.
Animal Study, published in iScience (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
- Animal Study
- Journal
- iScience (2026)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41959677
- DOI
- 10.1016/j.isci.2026.115280
Abstract (original English)
Severe acute pancreatitis (SAP) is a complex inflammatory disorder with severe immune imbalance. This study investigates the therapeutic potential of extracellular vesicles derived from human adipose mesenchymal stem cells (hADSC-EVs) in modulating Treg differentiation and alleviating SAP. We conducted a phosphoproteomics analysis to evaluate phosphorylation levels, and administered hADSC-EVs in a mouse model of SAP and assessed their impact on Treg differentiation. Phosphoproteomics revealed a significant increase in p-STK3 following hADSC-EVs treatment, restoring Foxp3 level diminished by STK3 knockdown. HADSC-EVs promoted Treg differentiation in a concentration-dependent manner by targeting Foxp3 transcription. In the SAP mouse model, hADSC-EVs improved survival rates and mitigated histopathological alterations. In conclusion, our study revealed that STK3 effectively promotes Treg differentiation and enhances their immunosuppressive capabilities, thereby ameliorating inflammation and attenuating the pathological phenotypes associated with SAP. These findings provide valuable insights into the potential role of hADSC-EVs in regulating immune responses and promoting tissue repair.
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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