ArticleCell metabolism2023
Oxylipin-PPARγ-initiated adipocyte senescence propagates secondary senescence in the bone marrow.
Article in Cell metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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87 citing papers in PubMed, 104 citations in OpenAlex.
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- Sulfated polysaccharide prevents senescent adipocyte-driven osteonecrosis by stem cell fate reprogramming.Bioactive materials · 2026Article
- Menaquinone-7 alleviates mitochondrial dysfunction and senescence in senile osteoporosis by targeting the PINK1-mediated mitophagy via PXR/ERK/CREB signaling pathway.Journal of pharmaceutical analysis · 2026Article
- Oxidized metabolites of linoleic acid as biomarkers of pancreatic beta-cell function in the first-onset type 2 diabetic patients with obesity.Journal of endocrinological investigation · 2026Article
- Targeting adipocyte ESRRA alleviates osteoarthritis via interrupting inter-organelle crosstalk of complement C3-CFD-MAC cascade.Bone research · 2026Article
- PPAR-γ suppresses macrophage senescence and allergic airway inflammation through controlling lipid metabolic pathways.EBioMedicine · 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
27 more citing papers are in PubMed but not listed here.
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9 authors at 1 institution in 1 country.
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Abstract
The chronic use of glucocorticoids decreases bone mass and quality and increases bone-marrow adiposity, but the underlying mechanisms remain unclear. Here, we show that bone-marrow adipocyte (BMAd) lineage cells in adult mice undergo rapid cellular senescence upon glucocorticoid treatment. The senescent BMAds acquire a senescence-associated secretory phenotype, which spreads senescence in bone and bone marrow. Mechanistically, glucocorticoids increase the synthesis of oxylipins, such as 15d-PGJ2, for peroxisome proliferator-activated receptor gamma (PPARγ) activation. PPARγ stimulates the expression of key senescence genes and also promotes oxylipin synthesis in BMAds, forming a positive feedback loop. Transplanting senescent BMAds into the bone marrow of healthy mice is sufficient to induce the secondary spread of senescent cells and bone-loss phenotypes, whereas transplanting BMAds harboring a p16INK4a deletion did not show such effects. Thus, glucocorticoid treatment induces a lipid metabolic circuit that robustly triggers the senescence of BMAd lineage cells that, in turn, act as the mediators of glucocorticoid-induced bone deterioration.
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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.