TL1A serves as a positive regulator to promote adipocyte differentiation.
Chang Z., Wang Q., Zhai Y., Li K., Zheng X., Wang Y.
Animal Study, published in PLoS One (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
- Animal Study
- Journal
- PLoS One (2026)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41712581
- DOI
- 10.1371/journal.pone.0343036
Abstract (original English)
Adipogenesis, the intricate process of differentiation from preadipocytes or mesenchymal stem cells into mature adipocytes, is crucial for the formation and metabolic function of adipose tissues in mammals. The TNF ligand-related molecule 1A (TL1A) is a type II transmembrane protein belonging to the TNF superfamily. Inflammation is involved in the whole process of adipocyte cell formation and obesity development. To investigate the potential influence of TL1A on adipocyte development, we examined mouse embryo fibroblasts (MEFs) and 3T3-L1 cells. Our findings indicated that TL1A-treated MEFs exhibited an elevated rate of spontaneous adipogenesis, with a significant enhancement in adipocyte formation upon induction with a combination of insulin, dexamethasone and methylisobutylxanthine. This increased adipogenesis was evidenced by augmented lipid droplet formation and elevated expression of several adipogenic markers. Specifically, there was an upregulation of early-stage adipogenesis genes, including Krox20, KLF5, C/EBPβ and C/EBPδ, as well as late-stage adipogenesis regulators such as KLF15, C/EBPα, PPARγ and aP2. Moreover, TL1A significantly upregulated the protein expression of adipogenic markers (C/EBPα, C/EBPβ, PPARγ, CD36 and aP2) in MEFs and 3T3-L1 cells. Mechanistically, TL1A enhanced the phosphorylation of yes-associated protein 1 (YAP1), which led to cytoplasmic retent
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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