Published online Nov 12, 2015. doi: 10.5499/wjr.v5.i3.127
Peer-review started: February 7, 2015
First decision: April 10, 2015
Revised: August 24, 2015
Accepted: September 7, 2015
Article in press: September 8, 2015
Published online: November 12, 2015
Processing time: 281 Days and 13.3 Hours
Rheumatoid arthritis (RA) is a systemic, inflammatory and autoimmune disorder, characterized by chronic arthritis with progressive joint destruction. It has a multifactorial aetiology involving both genetic and environmental factors. Epigenetics can be defined as modifications of DNA that result in altered gene expression. The two main epigenetic mechanisms are post translational modifications to histone tails and DNA methylation. Recent evidence has suggested that epigenetic mechanisms may be an important contributor to RA susceptibility. The aim of this editorial is to present evidence for the role of epigenetic mechanisms in the pathogenesis of RA and the potential to therapeutic target. Several studies targeting histone modification and DNA methylation in animal models of inflammatory arthritis will be reviewed and alterations in the epigenetic signature of genes of key RA related pathways such as pro-inflammatory cytokines, proteases and regulators of cellular proliferation.
Core tip: This paper has highlighted the numerous processes involved in the pathogenesis of rheumatoid arthritis (RA) that are modulated by epigenetic mechanisms. This is important hypotheses to explore a novel therapeutic target in RA.