miR-204-5p Promotes Hepatogenic Differentiation of Adipose-Derived Stem Cells to Ameliorate Acute Liver Failure via the MDM2/E2F8/BMP4 Axis.
Bi M., Dai B., Sha R., Hao X., Chen X., Du C.
Animal Study, published in FASEB J (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
- FASEB J (2026)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42273952
- DOI
- 10.1096/fj.202504415RR
Abstract (original English)
Acute liver failure (ALF) is characterized by extensive hepatocyte necrosis and limited treatment options. Adipose-derived stem cells (ADSCs) show potential for liver regeneration, yet the mechanisms regulating their hepatic differentiation remain unclear. Human ADSCs were infected with lentiviruses to overexpress or silence miR-204-5p, Murine double minute 2 (MDM2), E2F transcription factor 8 (E2F8), or bone morphogenetic protein 4 (BMP4). qPCR, immunofluorescence, and western blot detected mRNA and protein levels of hepatic markers-including hepatocyte nuclear factor 4 alpha (HNF4α), albumin (ALB), and alpha-fetoprotein (AFP). Periodic acid-Schiff (PAS) staining assessed glycogen storage, while enzyme-linked immunosorbent assay (ELISA) measured ALB and urea secretion. Dual-luciferase reporter and co-immunoprecipitation (Co-IP) assays verified molecular interactions and ubiquitination. A Carbon Tetrachloride (CCl₄)-induced ALF model in mice was adopted to investigate the therapeutic potential of miR-204-5p-overexpression ADSCs by fluorescence imaging, histology, tunel staining, and measurement of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. In vitro, miR-204-5p suppresses MDM2 expression, thereby reducing MDM2-mediated ubiquitination and degradation of E2F8. Stabilized E2F8 transcriptionally activates BMP4, ultimately promoting the hepatoge
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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