TAZ enhances the activity of the AKT signaling pathway to promote adipogenesis of gADSCs.
Zhou M., Zhang H., Miao X., Zhao Y., Zhu L., Liu J.
Animal Study, published in Stem Cell Res Ther (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
- Stem Cell Res Ther (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41013728
- PMCID
- PMC12465564
- DOI
- 10.1186/s13287-025-04640-8
Abstract (original English)
Adipose-derived mesenchymal stem cells (ADSCs) possess the capacity for multidirectional differentiation, including differentiation into adipocytes. However, the molecular mechanisms that control adipogenesis are not yet fully understood.Transcriptional co-activator with PDZ-binding motif (TAZ) can act as a molecular rheostat, finely regulating the balance between osteoblast and adipocyte differentiation. In this study, we investigated whether TAZ plays a role in the adipogenesis of goat ADSCs (gADCS). Our results indicated that the expression of TAZ increased during adipogenesis of gADSCs. We established gADSCs cell lines with stable TAZ overexpression and knockdown. We found that TAZ overexpression promoted the adipogenesis of gADSCs, whereas its knockdown inhibited this process. Furthermore, TAZ overexpression and knockdown altered the nuclear expression of Yes-associated protein(YAP) and TAZ. Subsequent analyses indicated that TAZ overexpression increased AKT phosphorylation levels. Moreover, treatment with a PI3K inhibitor (LY294002) abrogated the TAZ-induced increase in adipogenesis, suggesting that TAZ regulates the adipogenesis of gADSCs via the PI3K/AKT pathway. Collectively, our results indicate that TAZ promotes the adipogenesis of gADSCs by enhancing the activity of the PI3K/AKT signaling pathway.
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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