ArticleJournal of cellular and molecular medicine2025
Foxk2 Enhances Adipogenic Differentiation by Relying on the Transcriptional Activation of Peroxisome Proliferator-Activated Receptor Gamma.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Decoding the lncRNA landscape in bovine mastitis: insights into immune regulation and gene networks underlying host response.Journal of animal science and biotechnology · 2026Article
- TSPO governs bone-lipid homeostasis by redirecting BMSC differentiation via the PI3K/AKT/β-catenin pathway.Stem cell research & therapy · 2026Article
- Genome-wide association study of blood vitamin D metabolites and bone remodelling markers in pigs.BMC genomics · 2025Article
- Development and validation of machine learning-based diagnostic models using blood transcriptomics for early childhood diabetes prediction.Frontiers in medicine · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
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 feedback loop that drives adipogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.