ArticleAging2023
Development of a DNA damage-induced senescence model in osteoarthritic chondrocytes.
Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
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Who cites it
23 citing papers in PubMed, 22 citations in OpenAlex.
- SERPINE1/PAI-1 in Skeletal Degeneration: A Proposed Context-Dependent Framework for Bone Remodeling Regulation.Calcified tissue international · 2026Review
- Senescence-Associated Checkpoint Gene Dysregulation in Established Osteoarthritis: Integrated Transcriptomic Analysis and In Vitro Evaluation of CDK6 and WEE1.Biomedicines · 2026Article
- Article
- Cartilage targeted grape skin-derived extracellular vesicles ameliorate osteoarthritis by attenuating chondrocyte senescence.Journal of nanobiotechnology · 2026Article
- Comparative phenotypic and molecular profiling of replicative and chemically-induced senescence in articular chondrocytes.Cell death discovery · 2026Article
- Transcriptomic and Functional Comparison of Cells Isolated From Healthy and Degenerated Ovine Intervertebral Discs.Journal of cellular and molecular medicine · 2026Article
- Nanotherapeutic Strategies for Osteoarthritis: Targeting Aging, Metabolism and Inflammation.International journal of nanomedicine · 2026Review
- Targeting the senescence-associated secretory phenotype to modify osteoarthritis in aging.Inflammopharmacology · 2025Review
- FN9-10ELP, an ECM-Mimetic Fusion Protein, Protects Human Mesenchymal Stem Cells from Etoposide-Induced Senescence.International journal of molecular sciences · 2025Article
- The Senotherapeutic Effects of APPA (Apocynin [AP] and Paeonol [PA]) on Senescent Human Chondrocytes.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Cell-Surface LAMP1 is a Senescence Marker in Aging and Idiopathic Pulmonary Fibrosis.Aging cell · 2025Article
- Generation of an In Vitro Cartilage Aging Model Using Human Sera from Old Donors.Bioengineering (Basel, Switzerland) · 2025Article
- Development of Reliable and High-Throughput Human Biomimetic Cartilage and Bone Models to Explore Senescence and Personalized Osteoarthritis Treatment Options.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Article
- CPP-calcification of articular cartilage is associated with elevated cytokine levels in synovial fluid.Frontiers in cell and developmental biology · 2025Article
- Effects of MMP2 and its inhibitor TIMP2 on DNA damage, apoptosis and senescence of human lens epithelial cells induced by oxidative stress.Journal of bioenergetics and biomembranes · 2024Article
- Osteoarthritis: Insights into Diagnosis, Pathophysiology, Therapeutic Avenues, and the Potential of Natural Extracts.Current issues in molecular biology · 2024Review
- Aging and the emerging role of cellular senescence in osteoarthritis.Osteoarthritis and cartilage · 2024Review
- Article
- Roles of Microenvironment on Mesenchymal Stem Cells Therapy for Osteoarthritis.Journal of inflammation research · 2024Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescent cells (SnCs) have been described to accumulate in osteoarthritis (OA) joint tissues in response to injury, thereby participating in OA development and progression. However, clinical therapeutic approaches targeting SnCs using senolysis, although promising in preclinical OA models, have not yet proven their efficacy in patients with knee OA. This pitfall may be due to the lack of understanding of the mechanisms underlying chondrocyte senescence. Therefore, our study aimed to generate models of chondrocyte senescence. This study used etoposide, to induce DNA damage-related senescence or chronic exposure to IL-1β to entail inflammation-related senescence in human OA chondrocytes. Several hallmarks of cellular senescence, such as cell cycle arrest, expression of cyclin-dependent kinase inhibitors, DNA damages, and senescence-associated secretory profile were evaluated. Chronic exposure to IL-1β induces only partial expression of senescence markers and does not allow us to conclude on its ability to induce senescence in chondrocytes. On the other hand, etoposide treatment reliably induces DNA damage-related senescence in human articular chondrocytes evidenced by loss of proliferative capacity, DNA damage accumulation, and expression of some SASP components. Etoposide-induced senescence model may help investigate the initiation of cellular senescence in chondrocytes, and provide a useful model to develop therapeutic approaches to target senescence in OA.
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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.