ArticleBone research2022
IκB-ζ signaling promotes chondrocyte inflammatory phenotype, senescence, and erosive joint pathology.
Article in Bone research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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.
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Who cites it
46 citing papers in PubMed, 60 citations in OpenAlex.
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- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- Research progress on cellular senescence in the pathogenesis and treatment of osteoarthritis and temporomandibular joint osteoarthritis.Journal of oral & facial pain and headache · 2026Review
- Mechanisms and precision interventions in sarcopenia and osteoarthritis comorbidity: A narrative review.Journal of orthopaedic translation · 2026Review
- Cuttlefish ink nanoparticle hydrogels ameliorate osteoarthritis via concurrent inhibition of macrophage pyroptosis and chondrocyte senescence.Journal of nanobiotechnology · 2026Article
- Sulfated polysaccharide reprograms arterialized angiogenesis of endochondral ossification to rescue defective osteonecrosis therapy.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- cGAS-STING/HMGB1-mediated senescence induced by LRRK2 accelerates cartilage degeneration in osteoarthritis.Cell death & disease · 2026Article
- Ergothioneine prevents ovariectomy-induced osteoporosis by suppressing NF-κB/p65 signalling to attenuate osteoclastogenesis and bone marrow inflammation.Bone & joint research · 2026Article
- Recycling senescent cell lipids for targeted senotherapy.Nature communications · 2026Article
- Synergistic Effects of Nutritional Formula on Joint Inflammation Through Modulation of Bone Metabolism in Rats.Nutrients · 2026Article
- From mechanical triggering to metabolic-inflammatory driving: a new paradigm of knee osteoarthritis pathogenesis.Frontiers in immunology · 2026Review
- Crosstalk Between Inflammation and Cellular Senescence in Osteoarthritis: Modulatory Actions of Olive Oil and Its Bioactive Compounds.Mediators of inflammation · 2026Review
- Mechano-immune interactions in musculoskeletal aging: Mechanisms and translational perspectives.Theranostics · 2026Review
- Biomaterials targeting senescent cells for bone regeneration: State-of-the-art and future perspectives.Bioactive materials · 2025Review
- Targeting the senescence-associated secretory phenotype to modify osteoarthritis in aging.Inflammopharmacology · 2025Review
- Cross-regulation of inflammation and metabolic mechanisms in osteoarthritis: recent advances bridging the gap to novel treatments.Connective tissue research · 2025Review
- Crohn's Disease with Granulomatous Interstitial Nephritis as an Extraintestinal Complication from the Time of the Diagnosis.Internal medicine (Tokyo, Japan) · 2025Article
- Cellular senescence in age-related musculoskeletal diseases.Frontiers of medicine · 2025Review
- Mechanistic insights into Sanbi Decoction for osteoarthritis treatment based on network pharmacology and experimental validation.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Osteoarthritis is a joint disease characterized by a poorly-defined inflammatory response that does not encompass a massive immune cell infiltration yet contributes to cartilage degradation and loss of joint mobility, suggesting a chondrocyte intrinsic inflammatory response. Using primary chondrocytes from joints of osteoarthritic mice and patients, we first show that these cells express ample pro-inflammatory markers and RANKL in an NF-κB dependent manner. The inflammatory phenotype of chondrocytes was recapitulated by exposure of chondrocytes to IL-1β and bone particles, which were used to model bone matrix breakdown products revealed to be present in synovial fluid of OA patients, albeit their role was not defined. We further show that bone particles and IL-1β can promote senescent and apoptotic changes in primary chondrocytes due to oxidative stress from various cellular sources such as the mitochondria. Finally, we provide evidence that inflammation, oxidative stress and senescence converge upon IκB-ζ, the principal mediator downstream of NF-κB, which regulates expression of RANKL, inflammatory, catabolic, and SASP genes. Overall, this work highlights the capacity and mechanisms by which inflammatory cues, primarily joint degradation products, i.e., bone matrix particles in concert with IL-1β in the joint microenvironment, program chondrocytes into an "inflammatory phenotype" which inflects local tissue damage.
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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.