ArticleFrontiers in immunology2023
Inflammation produced by senescent osteocytes mediates age-related bone loss.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Consequences of Aging on Bone.Aging and disease · 2023Pooled it
- The role of the neuro-immune-bone axis in osteoporosis: from bone remodeling imbalance to multi-system interactions.Frontiers in immunology · 2026Review
- Cellular senescence in musculoskeletal diseases: biological mechanisms and clinical implications.Theranostics · 2026Review
- Aging-related metabolic dysregulation in osteoporosis: mechanisms and therapeutic strategies.Frontiers in aging · 2026Review
- Chronic low-grade inflammation drives skeletal aging and neurocognitive decline: inflammaging as a central hub coupling bone-brain aging.Frontiers in immunology · 2026Review
- Biomaterials targeting senescent cells for bone regeneration: State-of-the-art and future perspectives.Bioactive materials · 2025Review
- Musculoskeletal biomarkers in health and disease: implications for the aging spine-a review for spinal surgeons by the SRS adult spinal deformity task force on senescence.Spine deformity · 2025Review
- Recent Advances in the Role of Osteocytes in Orthodontic Tooth Movement.International journal of molecular sciences · 2025Review
- Immunoporosis: The hidden link between aging immune cells and bone fragility.Journal of orthopaedic translation · 2025Review
- Antisenescence therapies for age-related bone loss: Target factors, medicines, biomedical materials.Clinical and translational medicine · 2025Review
- Disulfidptosis and Its Hub Gene Slc3a2 Involved in Ulcerative Colitis Pathogenesis, Disease Progression, and Patient Responses to Biologic Therapies.International journal of molecular sciences · 2024Article
- Cellular senescence: A new perspective on the suppression of periodontitis (Review).Molecular medicine reports · 2024Review
- Hyperglycosylation as an Indicator of Aging in the Bone Metabolome ofMetabolites · 2024Article
- Ferroptosis in Osteocytes as a Target for Protection Against Postmenopausal Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Inflammatory Processes Affecting Bone Health and Repair.Current osteoporosis reports · 2023Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The molecular mechanisms of age-related bone loss are unclear and without valid drugs yet. The aims of this study were to explore the molecular changes that occur in bone tissue during age-related bone loss, to further clarify the changes in function, and to predict potential therapeutic drugs. Methods: We collected bone tissues from children, middle-aged individuals, and elderly people for protein sequencing and compared the three groups of proteins pairwise, and the differentially expressed proteins (DEPs) in each group were analyzed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). K-means cluster analysis was then used to screen out proteins that continuously increased/decreased with age. Canonical signaling pathways that were activated or inhibited in bone tissue along with increasing age were identified by Ingenuity Pathway Analysis (IPA). Prediction of potential drugs was performed using the Connectivity Map (CMap). Finally, DEPs from sequencing were verified by Western blot, and the drug treatment effect was verified by quantitative real-time PCR. Results: The GO and KEGG analyses show that the DEPs were associated with inflammation and bone formation with aging, and the IPA analysis shows that pathways such as IL-8 signaling and acute-phase response signaling were activated, while glycolysis I and EIF2 signaling were inhibited. A total of nine potential drugs were predicted, with rapamycin ranking the highest. In cellular experiments, rapamycin reduced the senescence phenotype produced by the H Conclusion: With age, inflammatory pathways are activated in bone tissue, and signals that promote bone formation are inhibited. This study contributes to the understanding of the molecular changes that occur in bone tissue during age-related bone loss and provides evidence that rapamycin is a drug of potential clinical value for this disease. The therapeutic effects of the drug are to be further studied in animals.
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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 Socratic graph.