M6A methylation modification in autoimmune diseases, a promising treatment strategy based on epigenetics

Arthritis Res Ther. 2023 Oct 2;25(1):189. doi: 10.1186/s13075-023-03149-w.

Abstract

Background: N6-methyladenosine (m6A) methylation modification is involved in the regulation of various biological processes, including inflammation, antitumor, and antiviral immunity. However, the role of m6A modification in the pathogenesis of autoimmune diseases has been rarely reported.

Methods: Based on a description of m6A modification and the corresponding research methods, this review systematically summarizes current insights into the mechanism of m6A methylation modification in autoimmune diseases, especially its contribution to rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE).

Results: By regulating different biological processes, m6A methylation is involved in the pathogenesis of autoimmune diseases and provides a promising biomarker for the diagnosis and treatment of such diseases. Notably, m6A methylation modification is involved in regulating a variety of immune cells and mitochondrial energy metabolism. In addition, m6A methylation modification plays a role in the pathological processes of RA, and m6A methylation-related genes can be used as potential targets in RA therapy.

Conclusions: M6A methylation modification plays an important role in autoimmune pathological processes such as RA and SLE and represents a promising new target for clinical diagnosis and treatment, providing new ideas for the treatment of autoimmune diseases by targeting m6A modification-related pathways.

Keywords: Autoimmune diseases; Methylation regulation; Rheumatoid arthritis; Systemic lupus erythematosus; m6a methylation modification.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Arthritis, Rheumatoid* / diagnosis
  • Arthritis, Rheumatoid* / genetics
  • Arthritis, Rheumatoid* / therapy
  • Autoimmune Diseases* / diagnosis
  • Autoimmune Diseases* / genetics
  • Autoimmune Diseases* / therapy
  • Epigenesis, Genetic / genetics
  • Humans
  • Lupus Erythematosus, Systemic* / diagnosis
  • Lupus Erythematosus, Systemic* / genetics
  • Lupus Erythematosus, Systemic* / therapy
  • Methylation