M2 macrophage-derived TGF-β induces age-associated loss of adipogenesis through progenitor cell senescence.
Zeng X., Wang TW., Yamaguchi K., Hatakeyama S., Yamazaki S., Shimizu E.
Animal Study, published in Mol Metab (2024) — 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
- Mol Metab (2024)
- Country
- Germany
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 38657734
- PMCID
- PMC11079528
- DOI
- 10.1016/j.molmet.2024.101943
- Citations
- 12
Abstract (original English)
Objectives Adipose tissue is an endocrine and energy storage organ composed of several different cell types, including mature adipocytes, stromal cells, endothelial cells, and a variety of immune cells. Adipose tissue aging contributes to the pathogenesis of metabolic dysfunction and is likely induced by crosstalk between adipose progenitor cells (APCs) and immune cells, but the underlying molecular mechanisms remain largely unknown. In this study, we revealed the biological role of p16 high senescent APCs, and investigated the crosstalk between each cell type in the aged white adipose tissue. Methods We performed the single-cell RNA sequencing (scRNA-seq) analysis on the p16 high adipose cells sorted from aged p16-Cre ERT2 /Rosa26-LSL-tdTomato mice. We also performed the time serial analysis on the age-dependent bulk RNA-seq datasets of human and mouse white adipose tissues to infer the transcriptome alteration of adipogenic potential within aging. Results We show that M2 macrophage-derived TGF-β induces APCs senescence which impairs adipogenesis in vivo. p16 high senescent APCs increase with age and show loss of adipogenic potential. The ligand-receptor interaction analysis reveals that M2 macrophages are the donors for TGF-β and the senescent APCs are the recipients. Indeed, treatment of APCs with TGF-β1 induces senescent phenotypes through mitochondrial ROS-mediated DNA dam
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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