ReviewFASEB bioAdvances2020
Current advances in regulation of bone homeostasis.
Review in FASEB bioAdvances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
87 citing papers in PubMed.
- Multiomics profiling of bone in the Dpp3-deficient mice unveils altered protein and lipid composition.Journal of endocrinological investigation · 2026Article
- Article
- Friedelin Enhances Gelatin/Nanohydroxyapatite Scaffold Performance by Inhibiting Osteoclastogenesis and Promoting Osteogenesis.ACS omega · 2026Article
- Biomaterial-assisted gene therapy for bone repair.Materials today. Bio · 2026Review
- Arginine Methylation Antagonizes TEAD3-Mediated Repression to Promote Osteogenic Differentiation by Disrupting RUNX2-Sequestrating Condensates.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- MicroRNA network regulation of developmental bone toxicity in a human embryonic stem cell osteogenic model.NAM journal · 2026Article
- Bone Marrow Mesenchymal Stromal Cell Osteogenesis is driven by Paracrine signals from Regulatory T Cell.Stem cell reviews and reports · 2026Article
- Senescence-associated secretory phenotype: the "pathogenic" factor driving orthopedic degenerative diseases and its regulation.Frontiers in aging · 2026Review
- Research advances and application prospects of CAR-T therapy in the treatment of age-related diseases.Frontiers in immunology · 2026Review
- Immune cell senescence and chronic bone diseases: osteoimmune mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Low-Dose Vitamin D3 Supplementation: Associations with Vertebral Fragility and Pedicle Screw Loosening.Journal of clinical medicine · 2025Article
- Phillygenin Improves the Focal Adhesion Kinase/Glycogen Synthase Kinase 3β/β-Catenin Axis to Promote Mesenchymal Stem Cell Osteogenic Differentiation.Phytotherapy research : PTR · 2025Article
- Human platelet-derived extracellular vesicle fractions modulate bone cell metabolism and biologize volume-stable β-TCP matrix in vitro.BMC medicine · 2025Article
- Increased BMP/SMAD Signaling by PD-MSCs Promotes Bone Formation in an Ovariectomized Mouse Model of Osteoporosis.International journal of molecular sciences · 2025Article
- Carnosine Biofunctionalized Hydroxyapatite Induces Copper-Driven Osteogenesis and Angiogenesis, Strengthening Its Bone Regenerative Capacities.ACS biomaterials science & engineering · 2025Article
- Carbohydrate-Rich Fraction of Aloe vera (L.) Burm.f. Extract Mitigates Bone Loss and Improves Metabolic Disturbance in Estrogen-Deficient Rats.Pharmacology research & perspectives · 2025Article
- RORβ Deficiency Inhibits Endochondral Ossification in Mice by Mediating the HIF-1α/VEGFA Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Article
- Bone Mineral Density in Children and Adolescents of the Abay Region, Kazakhstan: Prevalence and Associated Risk Factors.International journal of environmental research and public health · 2025Article
- Clustered peptide regulating the multivalent interaction between RANK and TRAF6 inhibits osteoclastogenesis by fine-tuning signals.Communications biology · 2025Article
27 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone homeostasis is securely controlled by the dynamic well-balanced actions among osteoclasts, osteoblasts and osteocytes. Osteoclasts are large multinucleated cells that degrade bone matrix and involve in the bone remodelling in conjunction with other bone cells, osteoblasts and osteocytes, the completely matured form of osteoblasts. Disruption of this controlling balance among these cells or any disparity in bone remodelling caused by a higher rate of resorption by osteoclasts over construction of bone by osteoblasts results in a reduction of bone matrix including bone mineral density (BMD) and bone marrow cells (BMCs). The dominating effect of osteoclasts results in advanced risk of bone crack and joint destruction in several diseases including osteoporosis and rheumatoid arthritis (RA). However, the boosted osteoblastic activity produces osteosclerotic phenotype and weakened its action primes to osteomalacia or rickets. On the other hand, senescent osteocytes predominately progress the senescence associated secretory phenotype (SASP) and may contribute to age related bone loss. Here, we discuss an advanced level work on newly identified cellular mechanisms controlling the remodelling of bone and crosstalk among bone cells as these relate to the therapeutic targeting of the skeleton.
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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 Socratic graph.