ReviewMolecules and cells2015
Epigenetic Regulation of Chondrocyte Catabolism and Anabolism in Osteoarthritis.
Review in Molecules and cells, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 72 citations in OpenAlex.
- Signal-driven interplay between lipid peroxidation and ferroptosis orchestrates osteoarthritis degeneration.Journal of orthopaedic translation · 2026Review
- Article
- Article
- Sophoridine attenuates osteoarthritis progression: association with suppression of chondrocyte pyroptosis via inhibiting NF-κB signaling pathway.Frontiers in pharmacology · 2026Article
- Blockade of ZMIZ1-GATA4 Axis Regulation Restores Youthfulness to Aged Cartilage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Bidirectional Role of Obesity and Aging in the Pathogenesis of Osteoarthritis: Molecular Mechanisms, Epigenetic Insights, and Therapeutic Implications.Journal of inflammation research · 2025Review
- Nutritional Epigenomics: Bioactive Dietary Compounds in the Epigenetic Regulation of Osteoarthritis.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Natural products in osteoarthritis treatment: bridging basic research to clinical applications.Chinese medicine · 2024Review
- Integrated Analysis of DNA Methylation and Gene Expression Profiles in a Rat Model of Osteoarthritis.International journal of molecular sciences · 2024Article
- Novel insights into the role of metabolic disorder in osteoarthritis.Frontiers in endocrinology · 2024Review
- Mitochondrial transfer balances cell redox, energy and metabolic homeostasis in the osteoarthritic chondrocyte preserving cartilage integrity.Theranostics · 2024Article
- The role of targeting glucose metabolism in chondrocytes in the pathogenesis and therapeutic mechanisms of osteoarthritis: a narrative review.Frontiers in endocrinology · 2024Review
- CircRREB1 mediates lipid metabolism related senescent phenotypes in chondrocytes through FASN post-translational modifications.Nature communications · 2023Article
- HTRA1 from OVX rat osteoclasts causes detrimental effects on endplate chondrocytes through NF-κB.Heliyon · 2023Article
- Mulberroside A alleviates osteoarthritis via restoring impaired autophagy and suppressing MAPK/NF-κB/PI3K-AKT-mTOR signaling pathways.iScience · 2023Article
- The epigenetic players and the chromatin marks involved in the articular cartilage during osteoarthritis.Frontiers in physiology · 2023Review
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- Article
- Current understanding of osteoarthritis pathogenesis and relevant new approaches.Bone research · 2022Review
- Epigenetic Regulation of Chondrocytes and Subchondral Bone in Osteoarthritis.Life (Basel, Switzerland) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is one of the most prevalent forms of joint disorder, associated with a tremendous socioeconomic burden worldwide. Various non-genetic and lifestyle-related factors such as aging and obesity have been recognized as major risk factors for OA, underscoring the potential role for epigenetic regulation in the pathogenesis of the disease. OA-associated epigenetic aberrations have been noted at the level of DNA methylation and histone modification in chondrocytes. These epigenetic regulations are implicated in driving an imbalance between the expression of catabolic and anabolic factors, leading eventually to osteoarthritic cartilage destruction. Cellular senescence and metabolic abnormalities driven by OA-associated risk factors appear to accompany epigenetic drifts in chondrocytes. Notably, molecular events associated with metabolic disorders influence epigenetic regulation in chondrocytes, supporting the notion that OA is a metabolic disease. Here, we review accumulating evidence supporting a role for epigenetics in the regulation of cartilage homeostasis and OA pathogenesis.
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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.