ArticleInternational journal of oral science2024
Multiomics profiling reveals VDR as a central regulator of mesenchymal stem cell senescence with a known association with osteoporosis after high-fat diet exposure.
Article in International journal of oral science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Molecular Mechanisms of Obesity-Associated Oxidative Stress and Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Review
- Epigenetic Mechanisms of Vitamin D in the Aging Process: A Narrative Review.International journal of molecular sciences · 2026Review
- Engineered probiotics constitutively expressing SOD alleviate inflammatory bowel disease by targeting ROS.iScience · 2026Article
- Vitamin D receptor signaling in inflammatory senescence-associated skin aging: Mechanisms and therapeutic potentials.Journal of cell communication and signaling · 2026Article
- Time-restricted feeding improves functional capacity of adipose-derived stem cells with activation of OSK-associated transcriptional programs.npj aging · 2026Article
- Bone Marrow Mesenchymal Stem Cell Senescence in the Development of Osteoporosis: Mechanisms, Interventions, and Future Directions.Current molecular medicine · 2026Review
- Bone formation niche dysfunction in osteoporosis: insights from single-cell and spatial transcriptomic studies.Frontiers in endocrinology · 2026Review
- Mesenchymal stem cell senescence as a potency brake: causes, consequences, and cures.Frontiers in aging · 2026Review
- VDR-Spermidine Axis Protects Against Age-Related Granulosa Cell Dysfunction and Follicular Decline via DNMTs-Mediated p53 Methylation.International journal of biological sciences · 2026Article
- Review
- Application of Machine Learning in Predicting Osteogenic Differentiation of Mesenchymal Stem Cells.Bioengineering (Basel, Switzerland) · 2025Review
- High-fat diet, intestinal microecology and bone loss.Nutrition & metabolism · 2025Review
- Activation of AKT1 enhances the capacity of senescent BMSCs to regulate osteoclast activation.Molecular medicine reports · 2025Article
- The Role of Senolytics in Osteoporosis.Biomolecules · 2025Review
- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 2025Review
- Cellular senescence in age-related musculoskeletal diseases.Frontiers of medicine · 2025Review
- NADProgress in orthodontics · 2025Article
- Exploring extracellular vesicles as novel therapeutic agents for intervertebral disc degeneration: delivery, applications, and mechanisms.Stem cell research & therapy · 2025Review
- Single-Cell Analysis Dissects the Effects of Vitamin D on Genetic Senescence Signatures Across Murine Tissues.Nutrients · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The consumption of a high-fat diet (HFD) has been linked to osteoporosis and an increased risk of fragility fractures. However, the specific mechanisms of HFD-induced osteoporosis are not fully understood. Our study shows that exposure to an HFD induces premature senescence in bone marrow mesenchymal stem cells (BMSCs), diminishing their proliferation and osteogenic capability, and thereby contributes to osteoporosis. Transcriptomic and chromatin accessibility analyses revealed the decreased chromatin accessibility of vitamin D receptor (VDR)-binding sequences and decreased VDR signaling in BMSCs from HFD-fed mice, suggesting that VDR is a key regulator of BMSC senescence. Notably, the administration of a VDR activator to HFD-fed mice rescued BMSC senescence and significantly improved osteogenesis, bone mass, and other bone parameters. Mechanistically, VDR activation reduced BMSC senescence by decreasing intracellular reactive oxygen species (ROS) levels and preserving mitochondrial function. Our findings not only elucidate the mechanisms by which an HFD induces BMSC senescence and associated osteoporosis but also offer new insights into treating HFD-induced osteoporosis by targeting the VDR-superoxide dismutase 2 (SOD2)-ROS axis.
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