Foxk2 Enhances Adipogenic Differentiation by Relying on the Transcriptional Activation of Peroxisome Proliferator-Activated Receptor Gamma.
Zhang S., You Y., Li R., Li M., Li Y., Yuan H.
Animal Study, published in J Cell Mol Med (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 Cell Mol Med (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 39789420
- DOI
- 10.1111/jcmm.70332
Abstract (original English)
Proper differentiation of bone marrow stromal cells (BMSCs) into adipocytes is crucial for maintaining skeletal homeostasis. However, the underlying regulatory mechanisms remain incompletely understood, posing a challenge for the treatment of age-related osteopenia and osteoporosis. Here, through comprehensive gene expression analysis during BMSC differentiation into adipocytes, we identified the forkhead transcription factor Foxk2 as a key regulator of this process. Foxk2 expression was significantly higher in the inguinal and epididymal white adipose tissues of db/db mice compared to non-obese db/m controls and was induced in BMSCs, C3H/10 T1/2, and ST2 cells following adipogenic stimulation. Overexpression of Foxk2 promoted adipogenic differentiation of C3H/10 T1/2, ST2, and BMSCs, accompanied by increased expression of lipogenic factors. Conversely, Foxk2 silencing inhibited adipogenic differentiation. Moreover, Foxk2 also facilitated lipogenesis of C3H/10 T1/2 and ST2 cells. Adipogenic stimuli triggered the nuclear translocation of Foxk2 through PI3-kinase and mTOR signalling pathways. Once in the nucleus, Foxk2 is directly bound to the promoters of Pparγ1 and Pparγ2, thereby enhancing their transcriptional activity. Notably, PPARγ1 and PPARγ2 reciprocally augmented the transcriptional activity of the Foxk2 promoter, indicating the presence of a Foxk2-PPARγ positive feedba
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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