RNA methylation: A potential therapeutic target in autoimmune disease

Autoimmune diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and inflammatory bowel disease (IBD) are caused by the body's immune response to autoantigens. The pathogenesis of autoimmune diseases is unclear. Numerous studies have demonstrated that RNA methylation plays a key role in disease progression, which is essential for post-transcriptional regulation and has gradually become a broad regulatory mechanism that controls gene expression in various physiological processes, including RNA nuclear output, translation, splicing, and noncoding RNA processing. Here, we outline the writers, erasers, and readers of RNA methylation, including N6-methyladenosine (m⁶A), 2'-O-methylation (Nm), 2'-O-dimethyladenosine (m⁶Am), N1-methyladenosine (m¹A), 5-methylcytidine (m⁵C) and N7-methylguanosine (m⁷G). As the role of RNA methylation modifications in the immune system and diseases is explained, the potential treatment value of these modifications has also been demonstrated. This review reports the relationship between RNA methylation and autoimmune diseases, highlighting the need for future research into the therapeutic potential of RNA modifications.