ReviewJBMR plus2021
Bone Aging, Cellular Senescence, and Osteoporosis.
Review in JBMR plus, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
123 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.
- Consequences of Aging on Bone.Aging and disease · 2023Pooled it
- Cellular senescence and the SASP in skeletal ageing: convergent mechanisms of progressive bone loss in osteoporosis.Biogerontology · 2026Review
- Naringin attenuates orchidectomy-induced bone loss in male rats: evidence from bone remodeling and telomere-related indices.Journal of molecular histology · 2026Article
- Bone as a Biomarker of Ageing and Senescence: Connecting Musculoskeletal Health to Longevity via Diet, Nutrition and Exercise.Biology · 2026Review
- A Review of Rejuvenation Strategies Targeting Mesenchymal Stem Cell Senescence and Their Impact on Bone Health and Regeneration.Current osteoporosis reports · 2026Review
- Expression of Senescence and Osteoporosis-Associated microRNAs in Human Bone and Their Correlations With Clinical Parameters of Osteoporotic Patients.Physiological research · 2026Article
- Inhibition of AXL receptor tyrosine kinase increases osteoblast function and bone mass.Bone research · 2026Article
- Later menopause confers no additional protection against osteoporosis in older women.Endocrine connections · 2026Article
- Biomarkers of Inflammaging and Cellular Senescence in Musculoskeletal (MSK) Diseases: The Knowns and the Unknowns.Biomedicines · 2026Article
- Intracellular Calcium Overload Promotes NFATc1-ATF3 Activation and Induces the Senescence-Associated Phenotype in Irradiated Osteocytes.Life (Basel, Switzerland) · 2026Article
- Therapeutic strategy for exosome-based bone regeneration to osteoporosis: Challenges and potential solutions.Journal of advanced research · 2026Review
- Review
- 3D morphological analysis of age and sex-related changes in human cortical bone remodeling spaces using micro-CT.Journal of anatomy · 2026Article
- 'Glucocorticoids, Cushing's syndrome and cellular senescence: a mechanistic link to metabolic ageing'.Endocrine connections · 2026Review
- 3D-printed titanium scaffolds coated with a multifunctional photothermal-responsive hydrogel promote osteoporotic bone defect repair.Materials today. Bio · 2026Article
- Bone Healing Around Implants in Normal and Medically Compromised Conditions: Osteoporosis and Diabetes.Advanced healthcare materials · 2026Review
- Bone Organoids as Advanced Models for Osteoporosis: Development, Application, and Future Prospects.International journal of molecular sciences · 2026Review
- The Role of Wnt Signaling in Age-Related Alveolar Bone Loss and Regeneration.Journal of periodontal research · 2026Review
- Sialin-STAT3 axis regulates bone homeostasis in mice.Bone research · 2026Article
- Force-Dependent Presence of Senescent Cells Expressing Vascular Endothelial Growth Factor During Orthodontic Tooth Movement.Biology · 2026Article
63 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Changes in aging bone that lead to osteoporosis are mediated at multiple levels, including hormonal alterations, skeletal unloading, and accumulation of senescent cells. This pathological interplay is superimposed upon medical conditions, potentially bone-wasting medications, modifiable and unmodifiable personal risk factors, and genetic predisposition that accelerate bone loss with aging. In this study, the focus is on bone hemostasis and its dysregulation with aging. The major physiological changes with aging in bone and the role of cellular senescence in contributing to age-related osteoporosis are summarized. The aspects of bone aging are reviewed including remodeling deficits, uncoupling phenomena, inducers of cellular senescence related to bone aging, roles of the senescence-associated secretory phenotype, radiation-induced bone loss as a model for bone aging, and the accumulation of senescent cells in the bone microenvironment as a predominant mechanism for age-related osteoporosis. The study also addresses the rationale and potential for therapeutic interventions based on the clearance of senescent cells or suppression of the senescence-associated secretory phenotype. © 2021 The Authors.
Indexed as
Identifiers
What OpenQuestion holds
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.