ArticleBioactive materials2025
Liver-bone organoids reveal senescence-driven interorgan crosstalk.
Article in Bioactive materials, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- MicroRNAs and Cellular Senescence in Melanoma: An Underexplored Link to Tumor Progression-A Systematic Review with Bioinformatics Analyses.International journal of molecular sciences · 2026Pooled it
- Bioactive glasses-mediated ion therapy ameliorates hepatic osteodystrophy by reprogramming the liver-bone axis.Bioactive materials · 2027Article
- Real-time sensing-integrated organoid-on-a-chip platforms: Technological progress and emerging biomedical applications.Bioactive materials · 2026Review
- The liver-bone axis: an emerging player in disease pathogenesis and therapeutic intervention.Science China. Life sciences · 2026Review
- O-GlcNAcylation: A bridge for regulating the function of the "heart-kidney-bone axis".Biochemistry and biophysics reports · 2026Review
- Organoids: generation strategies, applications, and future challenges.Stem cell research & therapy · 2026Review
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Authors and funding
16 authors.
Funding
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Abstract
The liver-bone axis plays a critical role in age-related diseases. However, current models inadequately capture its complex inter-organ communication. Here, we established novel, physiologically relevant senescent liver and bone organoid models using engineered bionic hydrogels combined with doxorubicin (DOX)-induced senescence. These models successfully recapitulated hallmark aging characteristics: bone organoids exhibited reduced mineralization accompanied by elevated senescence markers, and liver organoids demonstrated DNA damage along with structural deterioration. Notably, aged mouse serum effectively induced senescence in both organoid types, confirming the existence of systemic aging regulators. The platform demonstrated robust bidirectional crosstalk, with senescent liver organoid-conditioned medium potently driving degradation in bone organoids and senescent bone organoid-conditioned medium aggravating dysfunction in liver organoids. Mechanistically, we identified 27-hydroxycholesterol (27-OHC) as a novel hepatocyte-derived factor mediating liver-to-bone communication. 27-OHC not only induced bone organoids senescence but also synergized with DOX treatment to exacerbate bone loss, a finding corroborated by
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