Published in

Nature Research, Nature Reviews Rheumatology, 5(9), p. 311-318, 2013

DOI: 10.1038/nrrheum.2013.17



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The ascent of acetylation in the epigenetics of rheumatoid arthritis.

Journal article published in 2013 by Aleksander M. Grabiec ORCID, Kris A. Reedquist
This paper was not found in any repository; the policy of its publisher is unknown or unclear.
This paper was not found in any repository; the policy of its publisher is unknown or unclear.

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Genome-wide association studies have shown that genetic polymorphisms make a substantial but incomplete contribution to the risk of developing rheumatoid arthritis (RA). Efforts to understand the nongenetic contributions to RA disease susceptibility have recently focused on the study of epigenetic mechanisms, namely modifications of DNA and histones, which are subject to environmental influences and regulate gene expression. A surprising theme emerging from studies of the enzymes responsible for these epigenetic modifications, particularly histone deacetylases, is that they regulate inflammatory activation of cell populations relevant to RA through independent, direct, and dynamic interactions with nonhistone proteins. Herein, we highlight studies, the findings of which collectively suggest that revisiting the original definition of epigenetics, conceived some 70 years ago, might advance our interpretation of DNA and histone modifications with regard to gene expression and clinical outcome in RA. Such an approach could also facilitate the development of strategies to target these epigenetic modifications in the clinic.