ArticleJournal of cellular and molecular medicine2009
Involvement of SOX-9 and FGF-23 in RUNX-2 regulation in osteoarthritic chondrocytes.
Article in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.
- X-linked hypophosphatemia and spinal cord compression: a systematic review and illustrative case.Acta neurochirurgica · 2026Pooled it
- Osteoarthritis in the Elderly Population: Preclinical Evidence of Nutrigenomic Activities of Flavonoids.Nutrients · 2023Pooled it
- Therapeutic potential of SOX family transcription factors in osteoarthritis.Annals of medicine · 2025Review
- The Promising Role of Selected Fibroblast Growth Factors as Potential Markers of Complications in Type 1 and Type 2 Diabetes.International journal of molecular sciences · 2025Article
- Targeting Chondrocyte Hypertrophy as Strategies for the Treatment of Osteoarthritis.Bioengineering (Basel, Switzerland) · 2025Review
- Development of novel osteoarthritis therapy by targeting AMPK-β-catenin-Runx2 signaling.Genes & diseases · 2025Review
- Role of signaling pathways in age-related orthopedic diseases: focus on the fibroblast growth factor family.Military Medical Research · 2024Review
- Signalling interaction between β-catenin and other signalling molecules during osteoarthritis development.Cell proliferation · 2024Review
- Osteoarthritis versus psoriasis arthritis: Physiopathology, cellular signaling, and therapeutic strategies.Genes & diseases · 2024Review
- Collagen type II solution extracted from supercritical carbon dioxide decellularized porcine cartilage: regenerative efficacy on post-traumatic osteoarthritis model.Bioresources and bioprocessing · 2024Article
- Review
- FGF receptor inhibitor BGJ398 partially rescues osteoarthritis-like phenotype in older high molecular weight FGF2 transgenic mice via multiple mechanisms.Scientific reports · 2022Article
- Interdisciplinary management of FGF23-related phosphate wasting syndromes: a Consensus Statement on the evaluation, diagnosis and care of patients with X-linked hypophosphataemia.Nature reviews. Endocrinology · 2022Review
- Kindlin-2 preserves integrity of the articular cartilage to protect against osteoarthritis.Nature aging · 2022Article
- The anti-fibrotic agent nintedanib protects chondrocytes against tumor necrosis factor-ɑ (TNF-ɑ)-induced extracellular matrix degradation.Bioengineered · 2022Article
- Article
- Nrf2/ARE Signaling Directly Regulates SOX9 to Potentially Alter Age-Dependent Cartilage Degeneration.Antioxidants (Basel, Switzerland) · 2022Article
- HDAC4 mutant represses chondrocyte hypertrophy by locating in the nucleus and attenuates disease progression of posttraumatic osteoarthritis.BMC musculoskeletal disorders · 2022Article
- Longevity-Promoting Pathways and Transcription Factors Respond to and Control Extracellular Matrix Dynamics During Aging and Disease.Frontiers in aging · 2022Review
- Subchondral bone microenvironment in osteoarthritis and pain.Bone research · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chondrocytes' hypertrophy includes metabolic changes, matrix remodelling, proliferation and apoptosis, characteristics associated with the progression of osteoarthritis. We investigated a possible association among Runt-related transcription factor 2 (RUNX-2), SOX-9 and fibroblast growth factor (FGF)-23 mRNA expressions in articular chondrocytes in order to elucidate their contribution in the osteoarthritic hypertrophic cartilage. SOX-9, FGF-23, RUNX-2 and matrix metalloproteinase (MMP)-13 mRNA expressions were evaluated in osteoarthritic and normal chondrocytes by real-time PCR whereas MMP-13 protein expression by immunofluorescense. RUNX-2, FGF-23 and SOX-9 were down-regulated using small interfering RNA technology and transfection with liposomes. The effect of human recombinant FGF-23 (hrFGF-23) on SOX-9 and RUNX-2 expression was tested in normal chondrocytes. We found higher expression of RUNX-2 and FGF-23 and a decreased expression of SOX-9 mRNA in osteoarthritic chondrocytes compared to normal (P < 0.0001). RUNX-2 down-regulation resulted in reduced MMP-13 expression in osteoarthritic chondrocytes and inhibition of SOX-9 in increased RUNX-2 and MMP-13 mRNA expression in normal chondrocytes, whereas inhibition of FGF-23 resulted in reduced RUNX-2 mRNA expression in osteoarthritic chondrocytes (all P < 0.0001). Silencing of RUNX-2 or FGF-23 did not affect SOX-9 mRNA levels in osteoarthritic chondrocytes. Moreover simultaneous down-regulation of SOX-9 and up-regulation of FGF-23 mRNA expressions in normal chondrocytes resulted in additive up-regulation of RUNX-2 mRNA expression. Treatment of normal chondrocytes with hrFGF-23 resulted in increased RUNX-2 mRNA expression, whereas it had no effect on SOX-9 mRNA expression. We demonstrated convincing associations among RUNX-2, SOX-9 and FGF-23 in relation to MMP-13 expression in osteoarthritic chondrocytes, contributing to a better understanding of the abnormal gene expression and cartilage degeneration processes associated with 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 OpenQuestion graph.