Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016:2016:6290682.
doi: 10.1155/2016/6290682. Epub 2016 Dec 28.

The Mechanisms Underlying Chronic Inflammation in Rheumatoid Arthritis from the Perspective of the Epigenetic Landscape

Yasuto Araki  1 , Toshihide Mimura  1
Affiliations
Review

The Mechanisms Underlying Chronic Inflammation in Rheumatoid Arthritis from the Perspective of the Epigenetic Landscape

Yasuto Araki et al. J Immunol Res. 2016.

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease that is characterized by synovial hyperplasia and progressive joint destruction. The activation of RA synovial fibroblasts (SFs), also called fibroblast-like synoviocytes (FLS), contributes significantly to perpetuation of the disease. Genetic and environmental factors have been reported to be involved in the etiology of RA but are insufficient to explain it. In recent years, accumulating results have shown the potential role of epigenetic mechanisms, including histone modifications, DNA methylation, and microRNAs, in the development of RA. Epigenetic mechanisms regulate chromatin state and gene transcription without any change in DNA sequence, resulting in the alteration of phenotypes in several cell types, especially RASFs. Epigenetic changes possibly provide RASFs with an activated phenotype. In this paper, we review the roles of epigenetic mechanisms relevant for the progression of RA.

PubMed Disclaimer

Conflict of interest statement

The authors have no conflicting financial interests.

Figures

Figure 1
Figure 1
Epigenetic disorders induce the activation of rheumatoid arthritis synovial fibroblasts (RASFs). Normal SFs are differentiated from mesenchymal stromal or stem cells (MSCs) under normal epigenetic regulation in noninflammatory joints of healthy individuals. The activation of SFs is caused by aberrant epigenetic changes in inflammatory joints of RA.
See this image and copyright information in PMC

References

    1. Firestein G. S. Evolving concepts of rheumatoid arthritis. Nature. 2003;423(6937):356–361. doi: 10.1038/nature01661. - DOI - PubMed
    1. Gibofsky A. Epidemiology, pathophysiology, and diagnosis of rheumatoid arthritis: a synopsis. American Journal of Managed Care. 2014;20, S7:S128–S135. - PubMed
    1. Sakkas L. I., Bogdanos D. P., Katsiari C., Platsoucas C. D. Anti-citrullinated peptides as autoantigens in rheumatoid arthritis-relevance to treatment. Autoimmunity Reviews. 2014;13(11):1114–1120. doi: 10.1016/j.autrev.2014.08.012. - DOI - PubMed
    1. György B., Tóth E., Tarcsa E., Falus A., Buzás E. I. Citrullination: a posttranslational modification in health and disease. International Journal of Biochemistry and Cell Biology. 2006;38(10):1662–1677. doi: 10.1016/j.biocel.2006.03.008. - DOI - PubMed
    1. Young B. J. J., Mallya R. K., Leslie R. D., Clark C. J., Hamblin T. J. Anti-keratin antibodies in rheumatoid arthritis. British Medical Journal. 1979;2(6182):97–99. doi: 10.1136/bmj.2.6182.97. - DOI - PMC - PubMed