ReviewInternational journal of molecular sciences2019
NF-κB Signaling Regulates Physiological and Pathological Chondrogenesis.
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 papers.
What it found
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Who cites it
182 citing papers in PubMed, 310 citations in OpenAlex.
- Effects and mechanism of sestrin1 protein on osteoarthritis inflammation: A cellular model study.Irish journal of medical science · 2026Article
- Aerobic Exercise-Mediated Regulation of Ferroptosis in Skeletal Disorders: Molecular Mechanisms and Potential Applications.Biomolecules · 2026Review
- Contrasting Effects of HT-2 Toxin Exposure and ZIP6 Knockdown on Chondrocyte Extracellular Matrix Metabolism.Journal of biochemical and molecular toxicology · 2026Article
- Role of the immune microenvironment in bone regeneration and progress in immune-modulating bone nanobiomaterials.Journal of Zhejiang University. Science. B · 2026Review
- Emodin Attenuates Rheumatoid Arthritis by Modulating the NF-κB/HIF-1α/VEGF Signaling Pathway.International journal of molecular sciences · 2026Article
- Analysis of TNFAIP3, IRAK1, and TLR4 Gene Polymorphisms in Patients With Rheumatoid Arthritis.Immunity, inflammation and disease · 2026Article
- A comprehensive review on pain: Model, target, therapy, and prospect (Review).International journal of molecular medicine · 2026Review
- Insulin Resistance and Inflammation.International journal of molecular sciences · 2026Review
- Synovial transcriptome analysis reveals ShenTong ZhuYu Tang alleviates osteoarthritis by targeting MMP-9 and immune microenvironment.Journal of orthopaedic surgery and research · 2026Article
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- New Insights into the Role of NF-κB in Hepatitis B Virus Infection.International journal of biological sciences · 2026Review
- Neuro-immune-vascular-stem cell crosstalk in bone/cartilage regeneration: mechanisms, technological advances, and clinical perspectives.Frontiers in bioengineering and biotechnology · 2026Review
- NF-κB signaling in osteoarthritis: integrating mechanical stress, innate immunity, and cartilage degeneration.Frontiers in immunology · 2026Review
- Evaluation of the Effect of IL-1 Antagonists on Pituitary Function.International journal of endocrinology · 2026Article
- Integrating machine learning with SHAP to uncover multi-tissue molecular signatures in Osteoarthritis progression.PloS one · 2026Article
- Bmal1 Attenuates Collagen-Induced Arthritis by Regulating Macrophage Polarization via Sirt1.Journal of inflammation research · 2026Article
- The glycolytic enzyme PFKFB3 alleviates DNA damage and chondrocyte senescence in osteoarthritis.Cell death discovery · 2025Article
- Article
- Advances in the pathology and treatment of osteoarthritis.Journal of advanced research · 2025Review
- Integrated LC-MS/MS, Network Pharmacology, and Experimental Validation Reveal the Mechanism of Eucommia Ulmoides against Osteoarthritis.Cell biochemistry and biophysics · 2025Article
122 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
3 authors at 2 institutions in 1 country.
Funding
Abstract
The nuclear factor-κB (NF-κB) is a transcription factor that regulates the expression of genes that control cell proliferation and apoptosis, as well as genes that respond to inflammation and immune responses. There are two means of NF-κB activation: the classical pathway, which involves the degradation of the inhibitor of κBα (IκBα), and the alternative pathway, which involves the NF-κB-inducing kinase (NIK, also known as MAP3K14). The mouse growth plate consists of the resting zone, proliferative zone, prehypertrophic zone, and hypertrophic zone. The p65 (RelA), which plays a central role in the classical pathway, is expressed throughout the cartilage layer, from the resting zone to the hypertrophic zone. Inhibiting the classical NF-κB signaling pathway blocks growth hormone (GH) or insulin-like growth factor (IGF-1) signaling, suppresses cell proliferation, and suppresses bone morphogenetic protein 2 (BMP2) expression, thereby promoting apoptosis. Since the production of autoantibodies and inflammatory cytokines, such as tumor necrosis factor-α (TNFα), interleukin (IL)-1β, IL-6, and IL-17, are regulated by the classical pathways and are increased in rheumatoid arthritis (RA), NF-κB inhibitors are used to suppress inflammation and joint destruction in RA models. In osteoarthritis (OA) models, the strength of NF-κB-activation is found to regulate the facilitation or suppression of OA. On the other hand, RelB is involved in the alternative pathway, and is expressed in the periarticular zone during the embryonic period of development. The alternative pathway is involved in the generation of chondrocytes in the proliferative zone during physiological conditions, and in the development of RA and OA during pathological conditions. Thus, NF-κB is an important molecule that controls normal development and the pathological destruction of cartilage.
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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.