miR-19b-3p engineered adipose-derived stem cell exosomes attenuate acute liver failure via promoting tissue repair and microenvironment remodeling.
Wu B., Feng J., Wang X., Guo J., Sheng L., Wang J.
Animal Study, published in Mater Today Bio (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
- Mater Today Bio (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41560812
- PMCID
- PMC12813244
- DOI
- 10.1016/j.mtbio.2025.102697
Abstract (original English)
Acute liver failure (ALF) is a life-threatening clinical syndrome, characterized by rapid hepatocyte injury and deteriorating hepatic microenvironment. To date, there is still no effective clinical treatment for ALF. Adipose-derived stem cells (ADSCs) have been proven to be an ideal seed-cell in tissue engineering and regenerative medicine through ADSCs-derived exosomes (ADSC-EXO) by paracrine effect. Herein, we presented an ADSC-EXO based therapeutic strategy that could facilitate microenvironment reconstruction and tissue repairing simultaneously in ALF. We demonstrated that miR-19b-3p exhibited remarkable anti-inflammation and anti-oxidation effect. Functionalized exosomes miR-19-EXO administration elevated survival rates from 25 % to 75 %, concurrently reversing liver function, promoting histoarchitectural integrity, and ameliorating inflammatory infiltration in vivo . Mechanistically, miR-19b-3p directly targeted p47phox (a NADPH oxidase subunit) and impede hepatic oxidative stress level. Then, the redox homeostasis changes inactivated NF-κB pathway by impeding iKBα ubiquitination and blocking nuclear translocation of NF-κB P65, and then triggered the damping of M1 macrophage polarization. Notably, miR-19-EXO also outperformed lentiviral miR-19b-3p or shp47phox delivery and conventional ROS scavengers in synergistic biological functions. Our finding paves the way of engine
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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