ReviewOsteoarthritis and cartilage2024
Aging and the emerging role of cellular senescence in osteoarthritis.
Review in Osteoarthritis and cartilage, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses 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
74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.
- Nanomaterials targeting ferroptosis for osteoarthritis treatment: a systematic review of preclinical evidence.Journal of nanobiotechnology · 2026Pooled it
- Bibliometric analysis of research trends and emerging insights of osteoarthritis and chondrocyte hypertrophy.Frontiers in surgery · 2025Pooled it
- Stem cell senescence as a regenerative bottleneck in age-related skeletal degeneration: Mechanistic crosstalk and translational strategies.Regenerative therapy · 2026Review
- Research progress of mesenchymal stem cells/stromal cells and their derivatives against cell senescence in the treatment of osteoarthritis.Annals of medicine · 2026Review
- Traditional Chinese Medicine Formulas in Delaying Aging: From Theoretical Foundations to Molecular Mechanisms and Translational Perspectives.Journal of cellular and molecular medicine · 2026Review
- Low-power infrared laser on telomere maintenance in an experimental model of arthritis.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026Article
- Exercise alleviates age-related osteoarthritis associated with PGC-1α activation to suppress chondrocyte senescence and aberrant glycolysis.Journal of orthopaedic translation · 2026Article
- Network Model to Predict Age-Related Transcriptional Reprogramming.Aging cell · 2026Article
- Senescence-Associated Checkpoint Gene Dysregulation in Established Osteoarthritis: Integrated Transcriptomic Analysis and In Vitro Evaluation of CDK6 and WEE1.Biomedicines · 2026Article
- Determination of the most suitable reference gene for transcription analysis of synovial tissue from osteoarthritis patients.Scientific reports · 2026Article
- Biomarkers of Inflammaging and Cellular Senescence in Musculoskeletal (MSK) Diseases: The Knowns and the Unknowns.Biomedicines · 2026Article
- Identification of aging-related signature genes in temporomandibular joint degeneration based on bioinformatics.BMC oral health · 2026Article
- Synergistic targeting of senolytic and senomorphic action with dual-engineered biomimetic macrophage nanovesicles for mitigating osteoarthritis.Bioactive materials · 2026Article
- Cardiovascular health and osteoarthritis risk: a prospective cohort study with proteomic insights from UK Biobank.RMD open · 2026Article
- The common pathological network of inflammation, extracellular matrix imbalance, and senescence in intervertebral disc degeneration and osteoarthritis.Molecular biology reports · 2026Review
- NsPEFs-enriched ADSCs-EVs alleviate osteoarthritis via RSPO3-mediated dual pro-chondrogenic and pro-M2 macrophage properties.Bioactive materials · 2026Article
- Comparative whole-genome analyses of articular chondrocytes and skin fibroblasts reveal distinct genome instability landscapes in mesenchymal cell types.PLoS genetics · 2026Article
- p21 Knockdown as a Therapeutic Strategy for Focal Cartilage Injury Repair.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- [Protective effect and mechanism of TSPAN9-mediated mitocytosis in interleukin-1β-induced rat chondrocyte senescence].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026Article
- MEX3B aggravates osteoarthritis progression by post-transcriptionally activating TLR4-NF-κB signaling axis.Journal of orthopaedic surgery and research · 2026Article
14 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
objectiveThe correlation between age and incidence of osteoarthritis (OA) is well known but the causal mechanisms involved are not completely understood. This narrative review summarizes selected key findings from the past 30 years that have elucidated key aspects of the relationship between aging and OA.
methodsThe peer-reviewed English language literature was searched on PubMed using keywords including senescence, aging, cartilage, and osteoarthritis, for original studies and reviews published from 1993 to 2023 with a major focus on more recent studies. Manuscripts most relevant to aging and OA that examined one or more of the hallmarks of aging were selected for further review.
resultsAll proposed hallmarks of aging have been observed in articular cartilage and some have also been described in other joint tissues. Hallmarks include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, disabled macroautophagy, chronic inflammation, and dysbiosis. There is evidence that these age-related changes contribute to the development of OA in part by promoting cellular senescence. Senescence may therefore serve as a downstream mediator that connects numerous aging hallmarks to OA, likely through the senescence-associated secretory phenotype that is characterized by increased production of proinflammatory cytokines and matrix metalloproteinases.
conclusionsProgress over the past 30 years has provided the foundation for emerging therapies, such as senolytics and senomorphics, that hold promise for OA disease modification. Mechanistic studies utilizing physiologically-aged animals and cadaveric human joint tissues will be important for continued progress.
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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.