ArticleCell death & disease2022
Circular RNA circNFKB1 promotes osteoarthritis progression through interacting with ENO1 and sustaining NF-κB signaling.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Lactylation: a promising target for musculoskeletal disorders via interactions with chronic inflammation.Journal of advanced research · 2026Review
- Enolase 2-mediated lactylation-dependent disruption of the GNL3-MDM2-p53 axis in age-related osteoarthritis.Cellular & molecular biology letters · 2026Article
- Dysregulation of the glycolysis-mitochondrial metabolism axis in osteoarthritis: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2026Review
- Circular RNAs coordinate immunomodulation in osteoarthritic cartilage via antigen presentation and adaptive immune response.BMC musculoskeletal disorders · 2026Article
- NF-κB signaling in osteoarthritis: integrating mechanical stress, innate immunity, and cartilage degeneration.Frontiers in immunology · 2026Review
- Phosphatidylethanolamine Alleviates Osteoarthritis Progression by Inhibiting Oxidative Stress-Induced Chondrocyte Ferroptosis in a Lysosomal-Dependent Manner.International journal of general medicine · 2026Article
- Single-cell RNA sequencing generates an atlas of normal tibia cartilage under mechanical loading conditions.Molecular and cellular biochemistry · 2025Article
- Emerging role and clinical applications of circular RNAs in human diseases.Functional & integrative genomics · 2025Review
- 1,25(OH)Clinical rheumatology · 2025Article
- circ_0075048 silencing regulates LCP1 to improve IL-1β-induced chondrocyte injury by binding with miR-663b.Journal of orthopaedic surgery and research · 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
- Acid sensing to inflammaging: mechanisms and therapeutic promise of GPR68 (OGR1) in aging-related diseases.Frontiers in aging · 2025Review
- Integrating network pharmacology and experimental verification to explore the pharmacological mechanisms of phlorizin against osteoarthritis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Research progress of circRNAs in bone-related diseases.Frontiers in oncology · 2025Review
- Non-coding RNAs in osteoarthritis and osteoporosis-related hip fractures: molecular biomarkers for precision diagnosis and prognosis.Frontiers in endocrinology · 2025Review
- Article
- Post-Transcriptional Regulator RBM47 Stabilizes FBXO2 mRNA to Advance Osteoarthritis Development: WGCNA Analysis and Experimental Validation.Biochemical genetics · 2024Article
- Emerging technology has a brilliant future: the CRISPR-Cas system for senescence, inflammation, and cartilage repair in osteoarthritis.Cellular & molecular biology letters · 2024Review
- Noncoding RNAs in skeletal development and disorders.Biological research · 2024Review
- B7-H3 promotes proliferation and migration of lung cancer cells by modulating PI3K/AKT pathway via ENO1 activity.Translational cancer research · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory cytokines-induced activation of the nuclear factor κB (NF-κB) pathway plays a critical role in the pathogenesis of osteoarthritis (OA). Circular RNA (circRNA) has been identified as important epigenetic factor in numerous diseases. However, the biological roles of inflammation-related circRNAs in regulating OA pathogenesis remain elusive. Here, we revealed circRNA expression profiles in human primary chondrocytes with interleukin-1β (IL-1β) stimulation by circRNA sequencing. We identified a highly upregulated circRNA, termed as circNFKB1 in inflamed chondrocytes and osteoarthritic cartilage. As a circRNA derived from exon 2-5 of NFKB1, circNFKB1 is located in both cytoplasm and nucleus of chondrocytes. Furthermore, knockdown of circNFKB1 inhibited extracellular matrix (ECM) catabolism and rescued IL-1β impaired ECM anabolism whereas ectopic expression of circNFKB1 significantly promoted chondrocytes degradation in vitro. Moreover, intraarticular injection of adenovirus-circNFKB1 in mouse joints triggered spontaneous cartilage loss and OA development. Mechanistically, circNFKB1 interacted with α-enolase (ENO1), regulated the expression of its parental gene NFKB1 and sustained the activation of NF-κB signaling pathway in chondrocytes. Therefore, this study highlights a novel ENO1-interacting circNFKB1 in OA pathogenesis, and provides valuable insights into understanding the regulatory mechanism of NF-κB signaling in chondrocytes and a promising therapeutic target for the treatment of OA.
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