ReviewArthritis research2000
p53 in rheumatoid arthritis: friend or foe?
Review in Arthritis research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 15 citations in OpenAlex.
- MiR-199a-3p inhibits proliferation and induces apoptosis in rheumatoid arthritis fibroblast-like synoviocytes via suppressing retinoblastoma 1.Bioscience reports · 2018Article
- In vitro efficacy of polysaccharide-based nanoparticles containing disease-modifying antirheumatic drugs.Pharmaceutical research · 2014Article
- Mild electrical stimulation at 0.1-ms pulse width induces p53 protein phosphorylation and G2 arrest in human epithelial cells.The Journal of biological chemistry · 2013Article
- Evaluation of SV40-transformed synovial fibroblasts in the study of rheumatoid arthritis pathogenesis.Rheumatology international · 2012Article
- CIP2A expression is associated with synovial hyperplasia and invasive function of fibroblast-like synoviocytes in rheumatoid arthritis.Rheumatology international · 2012Article
- Cytoplasmic destruction of p53 by the endoplasmic reticulum-resident ubiquitin ligase 'Synoviolin'.The EMBO journal · 2007Article
- Discrepancy between mRNA and protein expression of tumour suppressor maspin in synovial tissue may contribute to synovial hyperplasia in rheumatoid arthritis.Annals of the rheumatic diseases · 2004Article
- Gene therapy in animal models of rheumatoid arthritis: are we ready for the patients?Arthritis research & therapy · 2004Review
- Gene therapy for arthritis.Gene therapy · 2003Review
- Molecular profile of synovial fibroblasts in rheumatoid arthritis depends on the stage of proliferation.Arthritis research · 2002Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The knowledge of transcription factors and proto-oncogenes has influenced the understanding of cell regulation, cell cycle, and apoptotic cell death in rheumatoid arthritis (RA) synovium. In addition, the development of normal synovial fibroblasts into transformed-appearing aggressive synovial fibroblasts may be triggered by the lack of antiproliferative factors, such as p53, p53-associated molecules, other tumor suppressors, as well as by upregulation of anti-apoptotic genes. Therefore, data derived from experiments such as those performed by Tak and colleagues in this issue of Arthritis Research not only enrich the intensive discussion addressing the impact of p53 on RA pathophysiology, they also may facilitate development of novel therapeutic approaches including p53-targeted gene therapy.
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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.