ArticleCell death & disease2023
Deciphering the interaction between Twist1 and PPARγ during adipocyte differentiation.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Regulatory risk loci link disrupted androgen response to the pathophysiology of polycystic ovary syndrome.Journal of the Endocrine Society · 2026Article
- Prussian blue analogue-mineralized ginseng-derived vesicles promote PPARγ nuclear translocation to suppress tumor vasculogenic mimicry and reverse the immunosuppressive microenvironment.Journal of nanobiotechnology · 2026Article
- Obesity disrupts ILC2 metabolic and functional homeostasis by inhibiting mTORC1 signaling.Cellular & molecular immunology · 2026Article
- The context-dependent roles of PPAR-γ in adipocyte differentiation and obesity: a master regulator with dual functions.Frontiers in nutrition · 2026Review
- Decoding the Function ofAnimals : an open access journal from MDPI · 2025Article
- Human miR-1 Stimulates Metabolic and Thermogenic-Related Genes in Adipocytes.International journal of molecular sciences · 2024Article
- Combined effects of genetic background and diet on mouse metabolism and gene expression.iScience · 2024Article
- The Impact of Resident Adipose Tissue Macrophages on Adipocyte Homeostasis and Dedifferentiation.International journal of molecular sciences · 2024Article
- Peroxisome proliferator-activated receptor gamma (PPAR-γ) activation through gut microbiota modulation as a novel therapeutic approach against anastomotic leak after colorectal cancer surgery.Journal of gastrointestinal oncology · 2024Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Obesity, a worldwide epidemic in recent years, is mainly due to the uncontrolled development of adipose tissues, which includes adipocyte hypertrophy and hyperplasia. Adipocyte differentiation is a process involving multiple transcription factor cascades, and the exact mechanism has not yet been defined. As a bHLH transcription factor, Twist1 exerts its activity by forming homo- or heterodimers with other factors. In this study, we showed Twist1 restricts adipogenesis through PPARγ. Expression of various differentiation markers (including PPARγ and adiponectin) and triglyceride-containing lipid droplets were decreased with overexpression of Twist1. Pathway enrichment analysis of RNA-seq data showed that differentially expressed genes (DEGs) caused by Twist1 overexpression were significantly related to lipolysis and PPARγ signaling. This implicates that Twist1 plays important regulatory roles in these processes. ChIP and dual luciferase assays showed that Twist1 could bind either PPARγ or adiponectin promoter to repress their respective transcription or directly to PPARγ protein to regulate its transcriptional activity. Furthermore, Twist1 directly interacted RXRα, which usually forms heterodimer with PPARγ to regulate adipogenesis. Taken together, our results suggest that Twist1 is an inhibitory modulator of adipogenesis and its function is likely through direct interaction with PPARγ protein or its gene promoter.
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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 OpenQuestion graph.