Nuclear Myosin 1 links genomic architecture to adipose tissue remodeling, metabolic inflammation and obesity in mice.
Khalaji S., Venit T., Lukáčová Z., Fambri V., Shrestha R., Kaluarachchi S.
Animal Study, published in Cell Death Dis (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
- Cell Death Dis (2026)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41748556
- DOI
- 10.1038/s41419-026-08525-3
Abstract (original English)
Adipocyte differentiation involves a metabolic transition from oxidative phosphorylation (OXPHOS) to aerobic glycolysis, allowing preadipocytes to meet the biosynthetic and energetic demands of maturation. Here, we show that nuclear myosin 1 (NM1), a chromatin-associated actomyosin motor, known to control transcription and chromatin accessibility, is required for metabolic homeostasis during adipocyte differentiation. Integrated ATAC-seq and RNA-seq profiling of NM1-deficient mouse embryonic fibroblasts (MEFs) revealed coordinated downregulation of key adipogenic and lipid-droplet machinery genes like Cebpa, Plin2, Abhd5, Agpat2, Pink1, and altered enhancer accessibility near adipogenesis-linked transcription factors (TFs) such as Klf6, Foxo3, Smad5, and Gata4. NM1 knockout (KO) mesenchymal stem cells (MSCs) exhibited impaired differentiation potential despite enlarged adipocyte morphology. In vivo, NM1-deficient mice developed progressive visceral obesity, accompanied by transcriptional reprogramming in epididymal white adipose tissue (eWAT), including repression of mitochondrial and adipogenic pathways and activation of inflammatory networks driven by IFNG, IL33, and TNF. Cross-species network analysis highlighted conserved regulatory architecture centered on MYO1C, implicating NM1/MYO1C as key chromatin-level regulators of adipose remodeling.
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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