TGF-β1-dependent expression of FOXS1 attenuates adipogenic potential and enhances a myofibroblast cellular phenotype.
Tavares AH., Connelly SP., Maksat D., Zheng J., Rabhi N., Layne MD.
Animal Study, published in J Biol Chem (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
- J Biol Chem (2025)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40774386
- PMCID
- PMC12423405
- DOI
- 10.1016/j.jbc.2025.110563
- Citations
- 2
Abstract (original English)
White adipose tissue (WAT) fibrosis is a major determinant of obesity-induced cardiometabolic dysfunction and is characterized by excessive extracellular matrix deposition and myofibroblast activation. Transforming growth factor (TGF)-β1 is a profibrotic cytokine that potently induces myofibroblast activation in adipocyte stem cells (ASCs). How TGF-β1 orchestrates ASC activation in WAT fibrosis is not completely understood. We identified FOXS1, a member of the forkhead box transcription factor superfamily, as a transcriptional target of TGF-β1 signaling in primary human WAT ASC (hASC). FOXS1 potentiated TGF-β1-dependent upregulation of several myofibroblast genes (e.g. Acta2, Col1a1, Fn1, and Il11) in 10T1/2 fibroblasts. FOXS1 also attenuated the induction of several adipogenic factors (e.g. Pparg, Stat5a, Fabp4, and Adipoq) in 10T1/2 fibroblasts and sensitized these cells to the antiadipogenic effects of TGF-β1. Furthermore, loss of endogenous FOXS1 improved adipogenic permissiveness and activated proadipogenic gene programs in 10T1/2 cells, even after TGF-β1 stimulation. These results indicate that FOXS1 is a positive regulator of profibrotic TGF-β1-dependent cellular responses, orchestrating the regulation of molecular phenotypes that promote myofibroblast activation and block adipogenesis. These findings offer novel insight into the TGF-β1-dependent roles of FOXS1 in fibrob
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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