ArticleCommunications biology2024
Inhibition of complement C3 prevents osteoarthritis progression in guinea pigs by blocking STAT1 activation.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
The trial behind it
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Immune dysregulation in osteoarthritis: Mechanisms, biomarkers, and therapeutic opportunities.Journal of translational autoimmunity · 2026Review
- Patient-Derived Transcriptomics Reveals Distinct IFNγ-Associated Myeloid States and Mitochondrial Complex I Programs in Rheumatoid Arthritis and Osteoarthritis.Biomedicines · 2026Article
- Plasma Proteomics Reveals Persistent and Surgery-Responsive Molecular Signatures in Osteoarthritis Patients.International journal of molecular sciences · 2026Article
- From bioinformatic identification to functional validation: MMP25 as a pro-inflammatory mediator in osteoarthritis.Journal of orthopaedic surgery and research · 2026Article
- Fexofenadine protects against osteoarthritis by targeting Smad2 and STAT1 to enhance anabolism and binding cPLA2 to inhibit catabolism.Cell death discovery · 2025Article
- iTRAQ proteomic analysis of exosomes derived from synovial fluid reveals disease patterns and potential biomarkers of Osteoarthritis.Journal of orthopaedic surgery and research · 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
7 authors at 1 institution in 2 countries.
Funding
Abstract
Osteoarthritis (OA) is one of the leading causes of disability, affecting over 500 million adults worldwide. Previous studies have found that various inflammatory factors can contribute to the pathogenesis of OA, including complement factors in the synovial fluid of OA patients. However, the pathogenesis of this disease is still not known, and the only therapy of severe OA is total joint replacements. Total joint replacements are invasive, expensive, and affect quality of life. Here we show that when human articular chondrocytes are stimulated with pro-inflammatory mediator interleukin-1β (IL-1β) there is an increase in inflammatory factors including complement component 3 (C3). We also found the transcription factor, signal transducer and activator of transcription 1 (STAT1), is responsible for increased C3 expression after IL-1β stimulation in human articular chondrocytes. A specific STAT1 inhibitor, fludarabine, attenuates the hyper-expression of C3 and delays/prevents spontaneous OA in Dunkin-Hartley guinea pigs. Since fludarabine is already clinically used for chemotherapy, this study has great translational potential as a unique disease-modifying osteoarthritis drug (DMOAD) in treating primary OA.
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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.