ArticleArthritis research & therapy2003
Functional analysis of an arthritogenic synovial fibroblast.
Article in Arthritis research & therapy, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 48 citations in OpenAlex.
- Effect of Antiseptic Irrigation Solutions on Primary Human Knee Fibroblasts Cultured in Human Platelet Lysate.The Journal of arthroplasty · 2025Article
- Circulating fibroblasts and neutrophils co-expressing CDH11Frontiers in immunology · 2025Article
- Integrated multi-omics for potential biomarkers and molecular mechanism of persistent inflammatory refractory rheumatoid arthritis.Frontiers in immunology · 2025Article
- Article
- Repurposing the antipsychotic drug amisulpride for targeting synovial fibroblast activation in arthritis.JCI insight · 2023Article
- Combination of subtherapeutic anti-TNF dose with dasatinib restores clinical and molecular arthritogenic profiles better than standard anti-TNF treatment.Journal of translational medicine · 2021Article
- Induction of chronic destructive arthritis in SCID mice by arthritogenic fibroblast-like synoviocytes derived from mice with antigen-induced arthritis.Arthritis research & therapy · 2018Article
- Comorbid TNF-mediated heart valve disease and chronic polyarthritis share common mesenchymal cell-mediated aetiopathogenesis.Annals of the rheumatic diseases · 2018Article
- Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.JCI insight · 2018Article
- Th17 in Animal Models of Rheumatoid Arthritis.Journal of clinical medicine · 2017Review
- IL-22 in tissue-protective therapy.British journal of pharmacology · 2013Review
- A metabolically-stabilized phosphonate analog of lysophosphatidic acid attenuates collagen-induced arthritis.PloS one · 2013Article
- Rheumatoid and pyrophosphate arthritis synovial fibroblasts induce osteoclastogenesis independently of RANKL, TNF and IL-6.Journal of autoimmunity · 2012Article
- Inflammation and bone destruction in arthritis: synergistic activity of immune and mesenchymal cells in joints.Frontiers in immunology · 2012Article
- Actin cytoskeleton dynamics linked to synovial fibroblast activation as a novel pathogenic principle in TNF-driven arthritis.Annals of the rheumatic diseases · 2007Review
- The ePHD protein SPBP interacts with TopBP1 and together they co-operate to stimulate Ets1-mediated transcription.Nucleic acids research · 2007Article
- Cytoskeletal rearrangements in synovial fibroblasts as a novel pathophysiological determinant of modeled rheumatoid arthritis.PLoS genetics · 2005Article
- [Research strategies towards a holistic characterization of rheumatoid arthritis--a systems biology approach].Zeitschrift fur Rheumatologie · 2005Review
- CD44 is a determinant of inflammatory bone loss.The Journal of experimental medicine · 2005Article
- Perspectives and limitations of gene expression profiling in rheumatology: new molecular strategies.Arthritis research & therapy · 2004Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing attention has been directed towards identifying non-T-cell mechanisms as potential therapeutic targets in rheumatoid arthritis. Synovial fibroblast (SF) activation, a hallmark of rheumatoid arthritis, results in inappropriate production of chemokines and matrix components, which in turn lead to bone and cartilage destruction. We have demonstrated that SFs have an autonomous pathogenic role in the development of the disease, by showing that they have the capacity to migrate throughout the body and cause pathology specifically to the joints. In order to decipher the pathogenic mechanisms that govern SF activation and pathogenic potential, we used the two most prominent methods of differential gene expression analysis, differential display and DNA microarrays, in a search for deregulated cellular pathways in the arthritogenic SF. Functional clustering of differentially expressed genes, validated by dedicated in vitro functional assays, implicated a number of cellular pathways in SF activation. Among them, diminished adhesion to the extracellular matrix was shown to correlate with increased proliferation and migration to this matrix. Our findings support an aggressive role for the SF in the development of the disease and reinforce the perspective of a transformed-like character of the SF.
Indexed as
Identifiers
What OpenQuestion holds
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.