ArticleJournal of cellular and molecular medicine2019
NOV/CCN3 induces cartilage protection by inhibiting PI3K/AKT/mTOR pathway.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 46 citations in OpenAlex.
- The Relationship Between CCN3 and Rheumatoid Arthritis and Its Potential Therapeutic Value.Journal of immunology research · 2026Review
- Emerging Role of Calycosin in Inflammatory Diseases: Molecular Mechanisms and Potential Therapeutic Applications.Biomolecules · 2025Review
- Critical Requirement of Senescence-Associated CCN3 Expression in CD44-Positive Stem Cells for Osteoarthritis Progression.International journal of molecular sciences · 2025Article
- HMGB1 Mediates Macrophage Recruitment and Regional Intervertebral Disc Properties Following Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Association of organs-crosstalk with the pathogenesis of osteoarthritis: cartilage as a key player.Frontiers in endocrinology · 2025Review
- Bottlebrush Polymers for Articular Joint Lubrication: Influence of Anchoring Group Chemistry on Lubrication Properties.ACS applied materials & interfaces · 2024Article
- Matricellular proteins: Potential biomarkers in head and neck cancer.Journal of cell communication and signaling · 2024Review
- Effect of a protein kinase B (Akt) inhibitor on the angiogenesis of HUVECs and corneal neovascularization.Wiener klinische Wochenschrift · 2024Article
- The advance of CCN3 in fibrosis.Journal of cell communication and signaling · 2023Review
- Association between endothelin-1 and systemic lupus erythematosus: insights from a case-control study.Scientific reports · 2023Article
- Blocking CCN2 Reduces Established Palmar Neuromuscular Fibrosis and Improves Function Following Repetitive Overuse Injury.International journal of molecular sciences · 2023Article
- Article
- CCN3/NOV Regulates Proliferation and Neuronal Differentiation in Mouse Hippocampal Neural Stem Cells via the Activation of the Notch/PTEN/AKT Pathway.International journal of molecular sciences · 2023Article
- Do not overwork: cellular communication network factor 3 for life in cartilage.Journal of cell communication and signaling · 2023Review
- Elevated Expression of CCN3 in Articular Cartilage Induces Osteoarthritis in Hip Joints Irrespective of Age and Weight Bearing.International journal of molecular sciences · 2022Article
- Icariin alleviates osteoarthritis through PI3K/Akt/mTOR/ULK1 signaling pathway.European journal of medical research · 2022Article
- Article
- High intratumoral dihydrotestosterone is associated with antiandrogen resistance in VCaP prostate cancer xenografts in castrated mice.iScience · 2022Article
- Integrative Analyses of Antler Cartilage Transcriptome and Proteome of Gansu Red Deer (Animals : an open access journal from MDPI · 2022Article
- Hierarchical functional nanoparticles boost osteoarthritis therapy by utilizing joint-resident mesenchymal stem cells.Journal of nanobiotechnology · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA), an age-related degenerative joint disease, is pathologically characterized by articular cartilage degeneration and synovial inflammation. Nephroblastoma overexpressed (NOV or CCN3), a matricellular protein, is a primary member of the CCN family (Cyr61, Ctgf, NOV) of proteins and is involved in various inflammatory disorders. Previous studies reported that CCN3 might play a therapeutic role in OA. However, the underlying mechanism remains unclear. In this study, we confirmed the expression of CCN3 was decreased in human and rat OA articular cartilage. Recombinant CCN3 ameliorated the IL-1β-induced matrix catabolism, as demonstrated by MMP1, MMP3, MMP13, ADAMTS5 and iNOS expression, in vitro. In addition, the degradation of cartilage matrix such as collagen 2 and aggrecan could be reversed by CCN3. Furthermore, we found CCN3 promoted autophagy as Atg5, Beclin1 and LC3-II expression were increased. High-mobility group box 1 was negatively correlated with CCN3 in IL-1β-induced osteoarthritis responses, and HMGB1 is involved in the protective effect of CCN3 in OA. Moreover, CCN3 overexpression decreased the expression of HMGB1 and reversed the IL-1β induced MMPs production. Additionally, recombinant CCN3 or CCN3 overexpression attenuated the activation of PI3K/AKT/mTOR pathway induced by IL-1β. Our study presents new mechanisms of CCN3 in osteoarthritis and indicates that CCN3 can serve as a novel potential therapeutic target for osteoarthritis.
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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 Socratic graph.