ReviewCurrent rheumatology reports2008
Cell death in osteoarthritis.
Review in Current rheumatology reports, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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
49 citing papers in PubMed, 106 citations in OpenAlex.
- Erianin protects chondrocytes against IL-1β-induced oxidative stress and ferroptosis by activating GPX4/STING signaling in osteoarthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Chondroitin sulfate alleviates osteoarthritis by upregulating HSPA8 to inhibit chondrocyte ferroptosis.PloS one · 2026Article
- Identification of ferroptosis-related genes and potential drugs in osteoarthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Chondrocyte Ferritinophagy as a Molecular Mechanism of Arthritis-A Narrative Review.Cell biochemistry and biophysics · 2025Review
- Therapeutic Controlled Release Strategies for Human Osteoarthritis.Advanced healthcare materials · 2025Review
- Using clustering of genetic variants in Mendelian randomization to interrogate the causal pathways underlying multimorbidity from a common risk factor.Genetic epidemiology · 2025Article
- CYR61 as a Potential Apoptosis Biomarker in Osteoarthritis with Comorbidities.Journal of musculoskeletal & neuronal interactions · 2024Article
- Biomarkers for hypertrophic chondrocyte differentiation are associated with spatial cellular organisation and suggest endochondral ossification-like processes in osteoarthritic cartilage: An exploratory study.Journal of orthopaedic translation · 2024Article
- TGF-β2 Induces Ribosome Activity, Alters Ribosome Composition and Inhibits IRES-Mediated Translation in Chondrocytes.International journal of molecular sciences · 2024Article
- Unraveling the path to osteoarthritis management: targeting chondrocyte apoptosis for therapeutic intervention.Frontiers in cell and developmental biology · 2024Review
- PPARγ activation suppresses chondrocyte ferroptosis through mitophagy in osteoarthritis.Journal of orthopaedic surgery and research · 2023Article
- Inflammatory cytokines and mechanical injury induce post-traumatic osteoarthritis-like changes in a human cartilage-bone-synovium microphysiological system.Arthritis research & therapy · 2022Article
- Article
- Sprifermin: Effects on Cartilage Homeostasis and Therapeutic Prospects in Cartilage-Related Diseases.Frontiers in cell and developmental biology · 2021Review
- Mitoprotective therapy prevents rapid, strain-dependent mitochondrial dysfunction after articular cartilage injury.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020Article
- Loganin Attenuates Osteoarthritis in Rats by Inhibiting IL-1β-Induced Catabolism and Apoptosis in Chondrocytes Via Regulation of Phosphatidylinositol 3-Kinases (PI3K)/Akt.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Mesenchymal Stem Cell Therapy for Osteoarthritis: The Critical Role of the Cell Secretome.Frontiers in bioengineering and biotechnology · 2019Review
- Cell sources of inflammatory mediators present in bone marrow areas inside the meniscus.PloS one · 2019Article
- Nanosome-Mediated Delivery Of Protein Kinase D Inhibitor Protects Chondrocytes From Interleukin-1β-Induced Stress And Apoptotic Death.International journal of nanomedicine · 2019Article
- Death of chondrocytes in Kashin-Beck disease: Apoptosis, necrosis or necroptosis?International journal of experimental pathology · 2018Article
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
To date, most studies examining cell death during the development of osteoarthritis (OA) have focused on death of chondrocytes and have primarily examined advanced stages of the disease. Very good evidence suggests that chondrocyte death does occur at some point in the pathogenesis of OA and that it can be due to apoptosis, necrosis, or some combination of the two. Chondrocyte death can be induced by mechanical injury, loss of extracellular matrix, loss of growth factors, or excessive levels of reactive oxygen species. Although therapy specifically targeting cell death in human OA has not been reported, preclinical studies in animal models have provided early evidence that inhibition of caspases might slow OA-like changes in articular cartilage. Because of potential unwanted side effects from agents systemically inhibiting cell death, treatments specifically targeting cell death in OA will likely need to be delivered locally and in a manner that prevents systemic absorption. Inhibition of cell death in OA likely will not be a sole therapeutic target but rather a desired effect of interventions designed to reverse the catabolic-anabolic imbalance occurring in OA joint tissues.
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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.