Autophagy-mediated regulation of hepatic differentiation of human adipose tissue-derived mesenchymal stem cells.
Niayesh-Mehr R., Piryaei A., Manafi A., Allameh A.
Laboratory Study, published in Int J Biochem Cell Biol (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
- Int J Biochem Cell Biol (2026)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41956356
- DOI
- 10.1016/j.biocel.2026.106929
Abstract (original English)
The regulation of mesenchymal stem cell (MSC) differentiation is a complex process influenced by multiple factors, among which autophagy has emerged as a key determinant of stem cell fate. Here, we investigated its role in MSC differentiation into hepatocyte-like cells. Autophagy was first assessed during basal hepatic differentiation of adipose tissue-derived MSCs (AD-MSCs) in the absence of modulators. Subsequently, we evaluated the impact of autophagy modulation by chemical agents on the functionality of the derived hepatocyte-like cells. Isolated AD-MSCs were induced to differentiate, and hepatocyte formation was assessed by morphological, molecular, and biochemical analyses. Macroautophagy was examined via protein and mRNA expression of key autophagy‑related markers, supplemented with transmission electron microscopy (TEM) and acridine orange staining. To confirm the role of autophagy in hepatic differentiation, differentiating MSCs were subjected to autophagy induction by serum starvation or treatment with rapamycin (50 nM), and inhibition using 3‑methyladenine (3‑MA, 5 µM). Autophagy activation was observed during baseline differentiation (days 0, 7, 14, and 21 post-induction), as indicated by increased Beclin‑1, LC3B, and ATG7 expression; reduced p62; and accumulation of autophagic vacuoles confirmed by TEM and acridine orange staining. Induction of autophagy by rapamyc
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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