ReviewRMD open2015
Pathophysiology of osteoarthritis: canonical NF-κB/IKKβ-dependent and kinase-independent effects of IKKα in cartilage degradation and chondrocyte differentiation.
Review in RMD open, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 121 citations in OpenAlex.
- Methylsulfonylmethane Improves Knee Quality of Life in Participants with Mild Knee Pain: A Randomized, Double-Blind, Placebo-Controlled Trial.Nutrients · 2023Trial
- Small heterodimer partner protects against osteoarthritis by inhibiting IKKβ/NF-κB-mediated matrix-degrading enzymes in chondrocytes.Nature communications · 2026Article
- NF-κB signaling in osteoarthritis: integrating mechanical stress, innate immunity, and cartilage degeneration.Frontiers in immunology · 2026Review
- Therapeutic potential of IκB kinase epsilon inhibition in preventing meniscal degeneration of early osteoarthritis.Bone & joint research · 2025Article
- Immunomodulation Effects of Porcine Cartilage Acellularized Matrix (pCAM) for Osteoarthritis Treatment.Tissue engineering and regenerative medicine · 2025Article
- Targeting TREM-1 receptors with metformin and pravastatin modulate monosodium iodoacetate-induced osteoarthritis.Inflammopharmacology · 2025Article
- Alternatively spliced NFKB1 transcripts enriched in Andean Aymara modulate inflammation, HIF and hemoglobin.Nature communications · 2025Article
- Association between ethylene oxide exposure and osteoarthritis risk among middle-aged and young adults: a cross-sectional study.Frontiers in public health · 2025Article
- siRNAs, tRNAs, and rRNAs in Osteoarthritis: Biological Functions and Therapeutic Opportunities.Biologics : targets & therapy · 2025Review
- A novel carboxamide bromodomain inhibitor attenuates osteoarthritis via epigenetic repression of NF-κB and MAPK signaling.Frontiers in immunology · 2025Article
- Chondroprotective functions of neutrophil-derived extracellular vesicles by promoting the production of secreted frizzled-related protein 5 in cartilage.Cell communication and signaling : CCS · 2024Article
- The emerging role of the semaphorin family in cartilage and osteoarthritis.Histochemistry and cell biology · 2024Review
- Emerging technology has a brilliant future: the CRISPR-Cas system for senescence, inflammation, and cartilage repair in osteoarthritis.Cellular & molecular biology letters · 2024Review
- Polynucleotides Suppress Inflammation and Stimulate Matrix Synthesis in an In Vitro Cell-Based Osteoarthritis Model.International journal of molecular sciences · 2023Article
- Breakthrough of extracellular vesicles in pathogenesis, diagnosis and treatment of osteoarthritis.Bioactive materials · 2023Review
- Lineage-specific differences and regulatory networks governing human chondrocyte development.eLife · 2023Article
- Drug Candidates for Autoimmune Diseases.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Article
- The essential anti-angiogenic strategies in cartilage engineering and osteoarthritic cartilage repair.Cellular and molecular life sciences : CMLS · 2022Review
- miR-17-92 cluster in osteoarthritis: Regulatory roles and clinical utility.Frontiers in genetics · 2022Review
8 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
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Osteoarthritis (OA), a whole-joint disease driven by abnormal biomechanics and attendant cell-derived and tissue-derived factors, is a rheumatic disease with the highest prevalence, representing a severe health burden with a tremendous economic impact. Members of the nuclear factor κB (NF-κB) family orchestrate mechanical, inflammatory and oxidative stress-activated processes, thus representing a potential therapeutic target in OA disease. The two pivotal kinases, IκB kinase (IKK) α and IKKβ, activate NF-κB dimers that might translocate to the nucleus and regulate the expression of specific target genes involved in extracellular matrix remodelling and terminal differentiation of chondrocytes. IKKα, required for the activation of the so-called non-canonical pathway, has a number of NF-κB-independent and kinase-independent functions in vivo and in vitro, including controlling chondrocyte hypertrophic differentiation and collagenase activity. In this short review, we will discuss the role of NF-κB signalling in OA pathology, with emphasis on the functional effects of IKKα that are independent of its kinase activity and NF-κB activation.
Indexed as
Identifiers
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.