ReviewArthritis research & therapy2012
Epigenetic contributions in the development of rheumatoid arthritis.
Review in Arthritis research & therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 74 citations in OpenAlex.
- CD5L insufficiency exacerbates skeletal joint damage in rheumatoid arthritis.Molecular medicine (Cambridge, Mass.) · 2026Article
- Epigenetic modifications of immune cells in rheumatoid arthritis.Annals of medicine · 2025Review
- Regulation of cytokine and chemokine expression by histone lysine methyltransferase MLL1 in rheumatoid arthritis synovial fibroblasts.Scientific reports · 2024Article
- DNA hypomethylation ameliorates erosive inflammatory arthritis by modulating interferon regulatory factor-8.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Electrospun Scaffold Micro-Architecture Induces an Activated Transcriptional Phenotype within Tendon Fibroblasts.Frontiers in bioengineering and biotechnology · 2021Article
- Identification of a Novel Serological Marker in Seronegative Rheumatoid Arthritis Using the Peptide Library Approach.Frontiers in immunology · 2021Article
- Hypermethylation of the miR-155 gene in the whole blood and decreased plasma level of miR-155 in rheumatoid arthritis.PloS one · 2020Article
- Trained Innate Immunity Not Always Amicable.International journal of molecular sciences · 2019Review
- Cimifugin Inhibits Inflammatory Responses of RAW264.7 Cells Induced by Lipopolysaccharide.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Pathologic Fibroblasts in Idiopathic Subglottic Stenosis Amplify Local Inflammatory Signals.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2019Article
- Suberoylanilide Hydroxamic Acid Attenuates Autoimmune Arthritis by Suppressing Th17 Cells through NR1D1 Inhibition.Mediators of inflammation · 2019Article
- Characterization of a Synovial B Cell-Derived Recombinant Monoclonal Antibody Targeting Stromal Calreticulin in the Rheumatoid Joints.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Evaluating the bromodomain protein BRD1 as a therapeutic target in rheumatoid arthritis.Scientific reports · 2018Article
- TNF inhibits catecholamine production from induced sympathetic neuron-like cells in rheumatoid arthritis and osteoarthritis in vitro.Scientific reports · 2018Article
- Right drug, right patient, right time: aspiration or future promise for biologics in rheumatoid arthritis?Arthritis research & therapy · 2017Review
- Article
- Inflammatory genes TNFα and IL6 display no signs of increased H3K4me3 in circulating monocytes from untreated rheumatoid arthritis patients.Genes and immunity · 2017Article
- Cellular and molecular pathways of structural damage in rheumatoid arthritis.Seminars in immunopathology · 2017Review
- Fibroblast-like synoviocyte metabolism in the pathogenesis of rheumatoid arthritis.Arthritis research & therapy · 2017Review
- Deregulation and therapeutic potential of microRNAs in arthritic diseases.Nature reviews. Rheumatology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is an autoimmune disease, characterized by chronic inflammation of the joints with severe pain and swelling, joint damage and disability, which leads to joint destruction and loss of function. Despite extensive research efforts, the underlying cause for RA is still unknown and current therapies are more or less effective in controlling symptoms but still fail to cure the disease. In recent years, epigenetic modifications were found to strongly contribute to the development of RA by affecting diverse aspects of the disease and modifying gene expression levels and behavior of several cell types, first and foremost joint resident synovial fibroblasts (SF). RASF are the most common cell type at the site of invasion. Owing to their aggressive, intrinsically activated phenotype, RASF are active contributors in joint damage. RASF are characterized by their ability to secrete cytokines, chemokines and joint-damaging enzymes. Furthermore, these cells are resistant to apoptosis, leading to hyperplasia of the synovium. In addition, RASF have invasive and migratory properties that could lead to spreading of the disease to unaffected joints. Epigenetic modifications, including DNA methylation and post-translational histone modifications, such as histone (de)acetylation, histone methylation and histone sumoylation were identified as regulatory mechanisms in controlling aggressive cell activation in vitro and in disease outcome in animal models in vivo. In the last 5 years, the field of epigenetics in RA has impressively increased. In this review we consider the role of diverse epigenetic modifications in the development of RA, with a special focus on epigenetic modifications in RASF.
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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.