Epigenetics in rheumatoid arthritis.

PURPOSE OF REVIEW

To give an overview of recently published articles addressing the role of epigenetic modifications in rheumatoid arthritis (RA). Here we focused on DNA methylation and posttranslational histone modifications.

RECENT FINDINGS

Recent studies attempted to link epigenetic modifications with genetic or environmental risk factors for RA. There is evidence that histone deacetylases confer effects of environmental triggers such as smoking, diet or therapy on expression levels of target genes. Additionally, disturbed methylation patterns and cell-type specific histone methylation marks were identified as potential mediators of genetic risk in RA. Altered methylome signatures were found in several cell types in RA, first of all RA synovial fibroblasts, and contribute to the intrinsic fibroblast activation. The reversal of DNA hypomethylation by inhibiting the polyamine recycling pathway was suggested as new epigenetic therapy in RA. Moreover, targeting epigenetic reader proteins, such as bromodomain proteins, emerged as a new field in drug development and the first studies underscored the potential of these drugs not only in malignant and inflammatory conditions but also in autoimmune diseases.

SUMMARY

Epigenetic factors represent a promising area to link genetics, regulation of gene expression and environmental risk factors.