ArticleNPJ Regenerative medicine2022
A STAT5-Smad3 dyad regulates adipogenic plasticity of visceral adipose mesenchymal stromal cells during chronic inflammation.
Article in NPJ Regenerative medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
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- Donor-matched iPSC model reveals context-dependent T2D genetic signals in fibro-adipogenic progenitors.bioRxiv : the preprint server for biology · 2026Article
- IFNγ and TNFα optimize salivary gland mesenchymal stromal cells: an alternative to marrow- and adipose-MSCs for radiation xerostomia.Regenerative therapy · 2025Article
- Activin Actions in Adipocytes.The Journal of clinical endocrinology and metabolism · 2025Review
- Exploring the nonlinear association between cardiometabolic index and hypertension in U.S. Adults: an NHANES-based study.BMC public health · 2025Article
- Analysis of TGFβ1-Induced activin A gene expression in kidney mesangial cells.Frontiers in molecular biosciences · 2025Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Adipogenic differentiation of visceral adipose tissue-resident multipotent mesenchymal stromal cells (VA-MSC) into adipocytes is metabolically protective. Under chronic inflammatory stress, this neoadipogenesis process is suppressed by various pro-inflammatory cytokines and growth factors. However, the underlying mechanism(s) regulating VA-MSC plasticity remains largely unexplored. Using an adipogenic differentiation screen, we identified IFNγ and TGFβ as key inhibitors of primary human VA-MSC differentiation. Further studies using human and mouse VA-MSCs and a chronic high-fat diet-fed murine model revealed that IFNγ/JAK2-activated STAT5 transcription factor is a central regulator of VA-MSC differentiation under chronic inflammatory conditions. Furthermore, our results indicate that under such conditions, IFNγ-activated STAT5 and TGFβ-activated Smad3 physically interact via Smad4. This STAT5-Smad4-Smad3 complex plays a crucial role in preventing the early adipogenic commitment of VA-MSCs by suppressing key pro-adipogenic transcription factors, including CEBPδ, CEBPα, and PPARγ. Genetic or pharmacological disruption of IFNγ-TGFβ synergy by inhibiting either STAT5 or Smad3 rescued adipogenesis under chronic inflammatory stress. Overall, our study delineates a central mechanism of MSC plasticity regulation by the convergence of multiple inflammatory signaling pathways.
Identifiers
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Registered trials
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