Extensive enhancer crosstalk controls PPARG2 activation during adipogenesis.
Cetnarowska A., Hyldahl M., Nygård M., Dashti H., Hansen BV., Holm LK.
Laboratory Study, published in Nat Commun (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
- Nat Commun (2026)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41832214
- DOI
- 10.1038/s41467-026-70401-7
Abstract (original English)
Transcriptional master regulators drive cell fate transitions. Peroxisome proliferator-activated receptor γ (PPARγ) is the master regulator of adipogenesis, and its expression must therefore be tightly regulated and efficiently induced in response to adipogenic cues. Here we decipher the regulatory mechanisms of the highly connected enhancer community driving activation of the PPARG locus during adipocyte differentiation of human mesenchymal stem cells. By systematically deleting nine individual enhancers, spanning upstream, promoter-proximal, and downstream super-enhancer constituents, we demonstrate elaborate enhancer crosstalk in cis involving stabilization of C/EBPβ recruitment prior to chromatin remodeling. We show that the super-enhancer constituent E + 102 plays a dual role in cis crosstalk and feedback activation and is obligate for activation of PPARG expression. Non-coding genetic variants associated with cardiometabolic traits and predicted to regulate PPARG expression map to E + 102 and other essential enhancers in the community, thereby supporting the importance of these enhancers in human physiology and disease.
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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