ArticleOsteoarthritis and cartilage2015
Targeted mutation of NOV/CCN3 in mice disrupts joint homeostasis and causes osteoarthritis-like disease.
Article in Osteoarthritis and cartilage, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Sex Specific Determinants in Osteoarthritis: A Systematic Review of Preclinical Studies.International journal of molecular sciences · 2020Pooled it
- Mechanobiology of Matricellular Proteins in Bladder Cancer: A Narrative Review and Bioinformatics Analysis.Biomolecules · 2026Review
- Species-specific roles of cellular communication network proteins in cartilage development: A comparative study using in vitro chondrogenic models.Journal of cell communication and signaling · 2026Article
- The Relationship Between CCN3 and Rheumatoid Arthritis and Its Potential Therapeutic Value.Journal of immunology research · 2026Review
- Critical Requirement of Senescence-Associated CCN3 Expression in CD44-Positive Stem Cells for Osteoarthritis Progression.International journal of molecular sciences · 2025Article
- Elevated Expression of CCN3 in Articular Cartilage Induces Osteoarthritis in Hip Joints Irrespective of Age and Weight Bearing.International journal of molecular sciences · 2022Article
- CCN proteins in the musculoskeletal system: current understanding and challenges in physiology and pathology.Journal of cell communication and signaling · 2021Review
- Cellular communication network factor 3 in cartilage development and maintenance.Journal of cell communication and signaling · 2021Review
- Targeting CCN Proteins in Rheumatoid Arthritis and Osteoarthritis.International journal of molecular sciences · 2021Review
- IL-12p40/IL-23p40 Blockade With Ustekinumab Decreases the Synovial Inflammatory Infiltrate Through Modulation of Multiple Signaling Pathways Including MAPK-ERK and Wnt.Frontiers in immunology · 2021Article
- CCN3 (NOV) Drives Degradative Changes in Aging Articular Cartilage.International journal of molecular sciences · 2020Article
- RNA-seq analysis of chondrocyte transcriptome reveals genetic heterogeneity in LG/J and SM/J murine strains.Osteoarthritis and cartilage · 2020Article
- Higher Serum CCN3 Is Associated with Disease Activity and Inflammatory Markers in Rheumatoid Arthritis.Journal of immunology research · 2020Article
- NOV/CCN3 induces cartilage protection by inhibiting PI3K/AKT/mTOR pathway.Journal of cellular and molecular medicine · 2019Article
- Review
- A friend in knee: CCN3 may inhibit osteoarthritis progression.Journal of cell communication and signaling · 2018Article
- Novel role of CCN3 that maintains the differentiated phenotype of articular cartilage.Journal of bone and mineral metabolism · 2017Article
- Understanding the pathophysiology of postpartum psychosis: Challenges and new approaches.World journal of psychiatry · 2017Review
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe matricellular protein NOV/CCN3, is implicated in osteoarthritis (OA) and targeted mutation of NOV in mice (Nov(del3)) leads to joint abnormalities. This investigation tested whether NOV is required for joint homeostasis and if its disruption causes joint degeneration.
methodNOV expression in the adult mouse joint was characterized by immunohistochemistry. A detailed comparison of the joints of Nov(del3)-/- and Nov(del3)+/+ (wild-type) males and females at 2, 6 and 12 months of age was determined by X-ray, histology and immunohistochemistry.
resultsNOV protein was found in specific cells in articular cartilage, meniscus, synovium and ligament attachment sites in adult knees. Nov(del3)-/- males exhibited severe OA-like pathology at 12 months (OARSI score 5.0 ± 0.5, P < 0.001), affecting all tissues of the joint: erosion of the articular cartilage, meniscal enlargement, osteophytic outgrowths, ligament degeneration and expansion of fibrocartilage. Subchondral sclerosis and changes in extracellular matrix composition consistent with OA, were also seen. The density of articular cartilage cells in Nov(del3)+/+ knee joints is maintained at a constant level from 2 to 12 months of age whereas this is not the case in Nov(del3)-/- mice. Compared with age and sex-matched Nov(del3)+/+ mice, a significant increase in articular cartilage density was seen in Nov(del3)-/- males at 2 months, whereas a significant decrease was seen at 6 and 12 months in both Nov(del3)-/- males and females.
conclusionNOV is required for the maintenance of articular cartilage and for joint homeostasis, with disruption of NOV in ageing Nov(del3)-/- male mice causing OA-like disease.
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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.