Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease hallmarked by progressive and irreversible joint destruction. RA pathogenesis is a T cell-regulated and B cell-mediated process in which activated lymphocyte-produced chemokines and cytokines promote leukocyte infiltration that ultimately leads to destruction of the joints. There is an obvious need to discover new drugs for RA treatment that have different biological targets or modes of action than the currently employed therapeutics. Environmental factors such as cigarette smoke, certain diet components, and oral pathogens can significantly affect gene regulation via epigenetic factors. Epigenetics opened a new field for pharmacology, and DNA methylation and histone modification-implicated factors are feasible targets for RA therapy. Exploring RA pathogenesis involved epigenetic factors and mechanisms is crucial for developing more efficient RA therapies. Here we review epigenetic alterations associated with RA pathogenesis including DNA methylation and interacting factors. Additionally, we will summarize the literature revealing the involved molecular structures and interactions. Finally, potential epigenetic factor-based therapies will be discussed that may help in better management of RA in the future.
Highlights
It is well established that gene expression is defined by cis-regulatory elements and trans-acting factors, and both of them can be directly or indirectly affected by epigenetic factors [1]
For practical use; epigenetic enzymes that establish, recognize, and remove DNA methylation can divided into three groups based on their catalytic activity; there are writers, readers, and be divided into three groups based on their catalytic activity; there are writers, readers, erasers
Steffen Gay’s lab in Zürich conducted one of the first epigenetic studies on RA synovial fibroblasts (RASFs), which was focused on a transposable element of the human genome (i.e., Line-1) that is silenced by DNA methylation in the promoter region [71]
Summary
It is well established that gene expression is defined by cis-regulatory elements and trans-acting factors, and both of them can be directly or indirectly affected by epigenetic factors [1]. CGIs are frequently evolutionary conserved sequences that promote gene expression by gene expression by regulating the chromatin structure and transcription factor binding. For practical use; epigenetic enzymes that establish, recognize, and remove DNA methylation can divided into three groups based on their catalytic activity; there are writers, readers, and be divided into three groups based on their catalytic activity; there are writers, readers, erasers. Epigenetic reprogramming events take place during the mammalian development, and they play an important role in writing the DNA methylation after the implantation of the blastocyst [8]. DNMT3A and DNMT3B enzymes that are capable of methylating DNA without any preference (Figure 2). Another protein called DNMT3-like (DNMT3L) is involved in the de novo methylation (Figure 2).
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call