ArticleGene2017
Old age and the associated impairment of bones' adaptation to loading are associated with transcriptomic changes in cellular metabolism, cell-matrix interactions and the cell cycle.
Article in Gene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
- Multi‑omics approaches to decipher the molecular mechanisms of exercise‑mediated bone protection: From mechanistic insights to personalized exercise prescription (Review).Molecular medicine reports · 2026Review
- Bone Aging and Glycative Stress: Convergent and Divergent Mechanisms Driving Skeletal Deterioration.Cells · 2026Review
- The Role of Wnt Signaling in Age-Related Alveolar Bone Loss and Regeneration.Journal of periodontal research · 2026Review
- The skeletal transcriptional response to mechanical load varies with age and tissue compartment in female mice.JBMR plus · 2025Article
- Bioenergetic programs of cancellous and cortical bone are distinct and differ with age and mechanical loading.Scientific reports · 2025Article
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- Genetic and Gene Expression Resources for Osteoporosis and Bone Biology Research.Current osteoporosis reports · 2023Review
- The Role of Bone Cell Energetics in Altering Bone Quality and Strength in Health and Disease.Current osteoporosis reports · 2023Review
- Network analysis reveals miRNA crosstalk between periodontitis and oral squamous cell carcinoma.BMC oral health · 2023Article
- Co-inhibition of ATM and ROCK synergistically improves cell proliferation in replicative senescence by activating FOXM1 and E2F1.Communications biology · 2022Article
- Cell energy metabolism and bone formation.Bone reports · 2022Article
- The mechanotransduction of MLO-Y4 cells is disrupted by the senescence-associated secretory phenotype of neighboring cells.Journal of cellular physiology · 2022Article
- Prioritization of Genes Relevant to Bone Fragility Through the Unbiased Integration of Aging Mouse Bone Transcriptomics and Human GWAS Analyses.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- Osteoblast-Specific Wnt Secretion Is Required for Skeletal Homeostasis and Loading-Induced Bone Formation in Adult Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- The Osteocyte Transcriptome: Discovering Messages Buried Within Bone.Current osteoporosis reports · 2021Review
- Genetic variability affects the skeletal response to immobilization in founder strains of the diversity outbred mouse population.Bone reports · 2021Article
- Biophysical Modulation of the Mitochondrial Metabolism and Redox in Bone Homeostasis and Osteoporosis: How Biophysics Converts into Bioenergetics.Antioxidants (Basel, Switzerland) · 2021Review
- Article
- Mechanotransduction via the coordinated actions of integrins, PI3K signaling and Connexin hemichannels.Bone research · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
In old animals, bone's ability to adapt its mass and architecture to functional load-bearing requirements is diminished, resulting in bone loss characteristic of osteoporosis. Here we investigate transcriptomic changes associated with this impaired adaptive response. Young adult (19-week-old) and aged (19-month-old) female mice were subjected to unilateral axial tibial loading and their cortical shells harvested for microarray analysis between 1h and 24h following loading (36 mice per age group, 6 mice per loading group at 6 time points). In non-loaded aged bones, down-regulated genes are enriched for MAPK, Wnt and cell cycle components, including E2F1. E2F1 is the transcription factor most closely associated with genes down-regulated by ageing and is down-regulated at the protein level in osteocytes. Genes up-regulated in aged bone are enriched for carbohydrate metabolism, TNFα and TGFβ superfamily components. Loading stimulates rapid and sustained transcriptional responses in both age groups. However, genes related to proliferation are predominantly up-regulated in the young and down-regulated in the aged following loading, whereas those implicated in bioenergetics are down-regulated in the young and up-regulated in the aged. Networks of inter-related transcription factors regulated by E2F1 are loading-responsive in both age groups. Loading regulates genes involved in similar signalling cascades in both age groups, but these responses are more sustained in the young than aged. From this we conclude that cells in aged bone retain the capability to sense and transduce loading-related stimuli, but their ability to translate acute responses into functionally relevant outcomes is diminished.
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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.