ArticleScientific reports2017
Epigenetic modifications of interleukin-6 in synovial fibroblasts from osteoarthritis patients.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 66 citations in OpenAlex.
- Trained immunity in chronic, relapsing and low-grade joint inflammation.Nature reviews. Rheumatology · 2026Review
- Methylation regulatory networks in osteoarthritis: mechanisms and targeted therapies.Journal of translational medicine · 2026Review
- Review
- A Narrative Review on Intra-Articular Injection Therapies for Knee Osteoarthritis: Current Evidence and Future Perspectives.Orthopedic research and reviews · 2026Review
- The mediation of circulating inflammatory proteins in the causal pathway from immune cells to osteoarthritis.Journal of orthopaedic surgery and research · 2025Article
- Osteoarthritis: Mechanisms and Therapeutic Advances.MedComm · 2025Review
- Article
- The Role of Exerkines in the Treatment of Knee Osteoarthritis: From Mechanisms to Exercise Strategies.Orthopaedic surgery · 2025Review
- Landscape of Histone Posttranslational Modifications in Osteoarthritis.Journal of inflammation research · 2025Review
- Clinical and omics biomarkers in osteoarthritis diagnosis and treatment.Journal of orthopaedic translation · 2025Review
- Nutritional Epigenomics: Bioactive Dietary Compounds in the Epigenetic Regulation of Osteoarthritis.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Matrix stiffness aggravates osteoarthritis progression through H3K27me3 demethylation induced by mitochondrial damage.iScience · 2024Article
- HLA-DRB1*15:01 and theNeurology(R) neuroimmunology & neuroinflammation · 2024Article
- The Killer's Web: Interconnection between Inflammation, Epigenetics and Nutrition in Cancer.International journal of molecular sciences · 2024Review
- Efficient generation of brain organoids using magnetized gold nanoparticles.Scientific reports · 2023Article
- Epigenetic regulation of 15-lipoxygenase-1 expression in human chondrocytes by promoter methylation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Inflammatory mechanisms in post-traumatic osteoarthritis: a role for CaMKK2.Immunometabolism (Cobham, Surrey) · 2023Review
- Unveiling the Genetic Footprint: Exploring Somatic Mutations in Peripheral Arterial Disease Progression.Biomedicines · 2023Review
- The Role of Genetics and Epigenetic Regulation in the Pathogenesis of Osteoarthritis.International journal of molecular sciences · 2023Review
- Post-traumatic osteoarthritis: A review of pathogenic mechanisms and novel targets for mitigation.Bone reports · 2023Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is the most common degenerative disease of the synovial joint. The synovial membrane is responsible for the inflammatory reaction leading to the secretion of macrophage-derived pro-inflammatory cytokines, such as IL-6. Suppressing IL-6 over-expression in synovial fibroblasts (SF) is a promising method to prevent OA development and progression, in which the prerequisite is the elucidation of the molecular mechanisms underlying IL-6 over-expression in SF. Currently, there are few reports concerning epigenetic modifications in IL-6 in OA SF. In the present study, we attempted to investigate this phenomenon. SF over-expressing IL-6 was collected from OA patients. DNA hypomethylation and histone hyperacetylation were observed in the IL-6 promoter regions in OA SF compared with normal SF. No differences in the status of H3K9 di-methylation, H3K27 tri-methylation and H3K4 tri-methylation were observed in the IL-6 promoter regions between normal and OA SF. DNA (cytosine-5-)-methyltransferase 3 alpha (Dnmt3a) overexpression and anacardic acid (histone acetyltransferase inhibitor) treatment increased DNA methylation and decreased histone acetylation in the IL-6 promoter, and IL-6 over-expression in OA SF was suppressed. These observations provide deeper insight into the pathogenesis of OA and can be used to design new drugs and develop new therapeutic methods to treat OA.
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