ArticleMedComm2025
Growth/Differentiation Factor 15 Promotes a Pro-Regenerative Response in Chondrocytes Upon Cartilage Injury.
Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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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Who cites it
5 citing papers in PubMed.
- Recent advances in biomarkers for cardiac fibrosis.Frontiers in cardiovascular medicine · 2026Review
- Targeting the CXCL12/CXCR4 pathway by an optimized derivative or EPI-X4 preserves chondrocyte function and offers a novel therapeutic approach in rheumatic diseases.Arthritis research & therapy · 2025Article
- Growth/Differentiation Factor 15 Promotes a Pro-Regenerative Response in Chondrocytes Upon Cartilage Injury.MedComm · 2025Article
- Intranasal Insulin Eases Autism in Rats via GDF-15 and Anti-Inflammatory Pathways.Current issues in molecular biology · 2024Article
- Terminal complement complex deposition on chondrocytes promotes premature senescence in age- and trauma-related osteoarthritis.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Posttraumatic osteoarthritis (PTOA) is a special form of osteoarthritis (OA), developing after joint injuries. Except for some minor clinical differences, no biologic marker has yet been identified to distinguish idiopathic OA (IOA) from PTOA. In this study, we investigated the expression of the stress-responsive cytokine growth differentiation factor 15 (GDF-15) in clinical samples from the Ulm OA study cohort and in a human ex vivo cartilage trauma model. GDF-15 levels were significantly higher in synovial fluid of PTOA patients as compared to IOA patients. We confirmed that fibroblast-like synoviocytes secreted GDF-15 after stimulation with medium of ex vivo-traumatized cartilage. Moreover, GDF-15 and its receptor, GFRAL, were elevated in highly degenerated OA cartilage. By means of a human cartilage trauma model, we discovered that chondrocytes produced GDF-15 upon tissue injury, while antioxidative treatment attenuated GDF-15 secretion. In fact, GDF-15 expression was mediated by oxidative stress and subsequent activation of p53. As a transcriptional target of p53, GDF-15 was associated with chondrosenescence. However, GDF-15 induced pro-regenerative response in chondrocytes, characterized by enhanced proliferation as well as chondro- and cell protection after cartilage trauma. Overall, this study first describes GDF-15 as a senescence-associated but potentially pro-regenerative cytokine in the context of human PTOA.
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Registered trials
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