ReviewThe journals of gerontology. Series A, Biological sciences and medical sciences2013
Basic biology of skeletal aging: role of stress response pathways.
Review in The journals of gerontology. Series A, Biological sciences and medical sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 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
101 citing papers in PubMed, 1 synthesis or guideline pooled it, 202 citations in OpenAlex.
- Metabolomic biomarkers of low BMD: a systematic review.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2021Pooled it
- Targeting the osteoporotic bone microenvironment: Mechanistic insight and therapeutic biomaterials for accelerating bone regeneration.Bioactive materials · 2026Review
- 'Glucocorticoids, Cushing's syndrome and cellular senescence: a mechanistic link to metabolic ageing'.Endocrine connections · 2026Review
- Alzheimer's Disease Risk Factor APOE4 Exerts Dimorphic Effects on Female Bone.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Interplay Between Bone Biology and Iron Metabolism: Molecular Mechanisms and Clinical Implications.Biomedicines · 2026Review
- Uncovering the Independent Role of Lipid Peroxidation in Osteoporosis Through an Integrated Bibliometric and Bioinformatics Analysis.Mediators of inflammation · 2026Article
- Osteoporosis: molecular pathogenesis and therapeutic interventions.Molecular biomedicine · 2025Review
- Human platelet-derived extracellular vesicle fractions modulate bone cell metabolism and biologize volume-stable β-TCP matrix in vitro.BMC medicine · 2025Article
- Characterizing aging-related genetic and physiological determinants of spinal curvature.Communications medicine · 2025Article
- Article
- Age-Related Oral and Para-Oral Tissue Disorders: The Evolving Therapeutic and Diagnostic Potential of Exosomes.Dentistry journal · 2025Review
- Therapeutic Potential of Bioactive Peptides Derived from Natural Products of Tortoiseshell and Antler in Alleviating Osteoporosis and Osteoarthritis.International journal of molecular sciences · 2025Article
- 37-Day microgravity exposure in 16-Week female C57BL/6J mice is associated with bone loss specific to weight-bearing skeletal sites.PloS one · 2025Article
- Potential threats of environmental microplastics to the skeletal system: current insights and future directions.Frontiers in endocrinology · 2025Review
- Role of lactoferrin in osteopenia and osteoporosis.Frontiers in nutrition · 2025Review
- Article
- Mitochondrial protein deacetylation by SIRT3 in osteoclasts promotes bone resorption with aging in female mice.Molecular metabolism · 2024Article
- MyD88 in osteoclast and osteoblast lineages differentially controls bone remodeling in homeostasis and malaria.International immunology · 2024Article
- Psychological Disorders Linked to Osteoporosis Diagnoses in a Population-Based Cohort Study of Middle and Older Age United States Adults.The Gerontologist · 2024Article
- METTL3-mediated m6A modification increases Hspa1a stability to inhibit osteoblast aging.Cell death discovery · 2024Article
41 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 at 1 institution in 1 country.
Funding
Abstract
Although a decline in bone formation and loss of bone mass are common features of human aging, the molecular mechanisms mediating these effects have remained unclear. Evidence from pharmacological and genetic studies in mice has provided support for a deleterious effect of oxidative stress in bone and has strengthened the idea that an increase in reactive oxygen species (ROS) with advancing age represents a pathophysiological mechanism underlying age-related bone loss. Mesenchymal stem cells and osteocytes are long-lived cells and, therefore, are more susceptible than other types of bone cells to the molecular changes caused by aging, including increased levels of ROS and decreased autophagy. However, short-lived cells like osteoblast progenitors and mature osteoblasts and osteoclasts are also affected by the altered aged environment characterized by lower levels of sex steroids, increased endogenous glucocorticoids, and higher oxidized lipids. This article reviews current knowledge on the effects of the aging process on bone, with particular emphasis on the role of ROS and autophagy in cells of the osteoblast lineage in mice.
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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.