ArticleScience signaling2021
IKKβ-NF-κB signaling in adult chondrocytes promotes the onset of age-related osteoarthritis in mice.
Article in Science signaling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 48 citations in OpenAlex.
- Structural and functional changes in articulating joints during aging of male and female C57BL/6JN mice.Osteoarthritis and cartilage · 2026Article
- Relative fat mass predicts symptomatic knee osteoarthritis in older adults with metabolic syndrome: a longitudinal cohort study.Journal of rehabilitation medicine · 2026Article
- Artemotil Attenuates Fibrosis-Associated Chondrocyte Remodelling in Osteoarthritis in Association With STC1-Related TGF-β/SMAD2/3 Signalling.Journal of cellular and molecular medicine · 2026Article
- Transcutaneous electrical nerve stimulation improves lateral ankle sprain (LAS) in rats by regulating the CXCL10/NF-kB signaling pathway: a potential treatment for LAS.Molecular biology reports · 2026Article
- Iron as a Key Mediator of Chronic Joint Damage: Insights from Hemophilic Arthropathy and Implications for Osteoarthritis.Medicina (Kaunas, Lithuania) · 2026Review
- A Principle-Guided Multistep Workflow for Screening Potential Quality Marker Candidates of Sanqi Shangyao Tablet Based on UHPLC-Q-Orbitrap MS, In Silico Screening, and In Vitro Validation.Biomedical chromatography : BMC · 2026Article
- Bioadhesive Hydrogel With Polyphenol-Armored Nanogene Rejuvenates Chondrocyte Senescence for Aged Osteoarthritis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- Crosstalk between autophagy and ferroptosis related genes in osteoarthritis: insights from transcriptomic and in vitro analyses.Irish journal of medical science · 2026Article
- Osteoarthritis: molecular pathogenesis and potential therapeutic options.Signal transduction and targeted therapy · 2026Review
- Small heterodimer partner protects against osteoarthritis by inhibiting IKKβ/NF-κB-mediated matrix-degrading enzymes in chondrocytes.Nature communications · 2026Article
- LOXL2 deletion triggers TMJ osteoarthritis, while overexpression protects it from NF-κB-induced chondrocyte apoptosis.International journal of oral science · 2026Article
- Article
- A sulfate-arsenical-ferruginous water affects apoptosis, oxidative stress and the gene expression of inflammatory mediators and of a panel of MicroRNA in IL-1β stimulated human osteoarthritic chondrocytes.Frontiers in medicine · 2026Article
- Senescence-associated secretory phenotype: the "pathogenic" factor driving orthopedic degenerative diseases and its regulation.Frontiers in aging · 2026Review
- From mechanical triggering to metabolic-inflammatory driving: a new paradigm of knee osteoarthritis pathogenesis.Frontiers in immunology · 2026Review
- Apigenin accelerates fracture healing by enhancing endochondral differentiation and inflammation resolution via targeting NF-κB signaling.Frontiers in immunology · 2026Article
- Personalizing fall fear prevention in knee osteoarthritis: an interpretable prediction framework via IGKSO synchronous optimization and SHAP-based risk stratification.Frontiers in public health · 2026Article
- Targeting the senescence-associated secretory phenotype to modify osteoarthritis in aging.Inflammopharmacology · 2025Review
- Severe osteoarthritis in aged PANX3 knockout mice: implications for a novel primary osteoarthritis model.JBMR plus · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Canonical nuclear factor κB (NF-κB) signaling mediated by homo- and heterodimers of the NF-κB subunits p65 (RELA) and p50 (NFKB1) is associated with age-related pathologies and with disease progression in posttraumatic models of osteoarthritis (OA). Here, we established that NF-κB signaling in articular chondrocytes increased with age, concomitant with the onset of spontaneous OA in wild-type mice. Chondrocyte-specific expression of a constitutively active form of inhibitor of κB kinase β (IKKβ) in young adult mice accelerated the onset of the OA-like phenotype observed in aging wild-type mice, including degenerative changes in the articular cartilage, synovium, and menisci. Both in vitro and in vivo, chondrocytes expressing activated IKKβ had a proinflammatory secretory phenotype characterized by markers typically associated with the senescence-associated secretory phenotype (SASP). Expression of these factors was differentially regulated by p65, which contains a transactivation domain, and p50, which does not. Whereas the loss of p65 blocked the induction of genes encoding SASP factors in chondrogenic cells treated with interleukin-1β (IL-1β) in vitro, the loss of p50 enhanced the IL-1β–induced expression of some SASP factors. The loss of p50 further exacerbated cartilage degeneration in mice with chondrocyte-specific IKKβ activation. Overall, our data reveal that IKKβ-mediated activation of p65 can promote OA onset and that p50 may limit cartilage degeneration in settings of joint inflammation including advanced age.
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