ArticleeLife2022
Osteocytes regulate senescence of bone and bone marrow.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 82 citations in OpenAlex.
- ANGPTL8 induces the aging of hematopoietic stem/progenitor cells.Biogerontology · 2026Article
- Apoptosis of Mdm2-deficient osteocytes enhances osteogenesis through TRPM8-enriched apoptotic vesicles.Bone research · 2026Article
- PCET-Inspired Nanoparticles Enable Paired Proton-Electron Delivery to Restore Mitochondrial Electron Transport and Regenerate Bone During Aging.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Chondrocytes in fracture healing: A review of chondrocyte journey.Chinese medical journal · 2026Review
- Genomic structural equation modeling reveals the shared genetic architecture of osteosarcopenia across five musculoskeletal phenotypes.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Development-based In Vivo Bioreactor Strategy for Challenging Senescent Bone Reconstruction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Osteocytes in the Metastatic Bone Niche: Mechanistic Pathways and Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Osteolineage cells ablation promotes skin aging phenotypes via dysregulated bone marrow macrophages.iScience · 2026Article
- Reduced osteogenic factors and early osteoblast senescence in SOD1(G93A) ALS mouse model.JCI insight · 2026Article
- The Mechanical Microenvironment of Trabecular Bones Subjected to a Physiological Gait Load.Annals of biomedical engineering · 2026Article
- Immune ageing in skeletal fragility: clonal haematopoiesis and failure of inflammatory resolution during fracture repair.Frontiers in immunology · 2026Review
- Development and evaluation of a machine learning based risk prediction model for osteoporosis.Frontiers in molecular biosciences · 2026Article
- Chronic low-grade inflammation drives skeletal aging and neurocognitive decline: inflammaging as a central hub coupling bone-brain aging.Frontiers in immunology · 2026Review
- Osteoimmune senescence in aging bone: from inflammaging dogma to cell-type-specific therapeutic windows.Frontiers in immunology · 2026Review
- Senescent immune cells, inflammaging, and bone loss: therapeutic potential and translational challenges of senolytics in osteoporosis.Frontiers in endocrinology · 2026Review
- The talin1-p53 axis inhibits osteocyte senescence to promote bone mass and mediate skeletal adaptation to mechanical stimulation.Theranostics · 2026Article
- The Crosstalk Between B Cells and the Skeletal System During Development, Aging, and in Pathological Conditions.Current osteoporosis reports · 2025Review
- Biofunctionalization of Stem Cell Scaffold for Osteogenesis and Bone Regeneration.Biomolecules · 2025Review
- Article
- Biomaterials targeting senescent cells for bone regeneration: State-of-the-art and future perspectives.Bioactive materials · 2025Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The skeletal system contains a series of sophisticated cellular lineages arising from the mesenchymal stem cells (MSCs) and hematopoietic stem cells (HSCs) that determine the homeostasis of bone and bone marrow. Here, we reasoned that osteocyte may exert a function in regulation of these lineage cell specifications and tissue homeostasis. Using a mouse model of conditional deletion of osteocytes by the expression of diphtheria toxin subunit α in dentin matrix protein 1 (DMP1)-positive osteocytes, we demonstrated that partial ablation of DMP1-positive osteocytes caused severe sarcopenia, osteoporosis, and degenerative kyphosis, leading to shorter lifespan in these animals. Osteocytes reduction altered mesenchymal lineage commitment, resulting in impairment of osteogenesis and induction of osteoclastogensis. Single-cell RNA sequencing further revealed that hematopoietic lineage was mobilized toward myeloid lineage differentiation with expanded myeloid progenitors, neutrophils, and monocytes, while the lymphopoiesis was impaired with reduced B cells in the osteocyte ablation mice. The acquisition of a senescence-associated secretory phenotype (SASP) in both osteogenic and myeloid lineage cells was the underlying cause. Together, we showed that osteocytes play critical roles in regulation of lineage cell specifications in bone and bone marrow through mediation of senescence.
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Registered trials
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.