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Review Article | Open Access

The role of m6A RNA methylation in autoimmune diseases: Novel therapeutic opportunities

Yunan Shana,b, Wei Chenc( ), Yanbin Lib( )
The First Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250013, China
Department of Neurology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Institute of Neuroimmunology, Shandong Key Laboratory of Rheumatic Disease and Translational Medicine, Jinan, Shandong 250013, China
Department of Gastroenterology, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200233, China

Peer review under responsibility of Chongqing Medical University.

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Abstract

N6-methyladenosine (m6A) modifications, as one of the most common forms of internal RNA chemical modifications in eukaryotic cells, have gained increasing attention in recent years. The m6A RNA modifications exert various crucial roles in various biological processes, such as embryonic development, neurogenesis, circadian rhythms, and tumorigenesis. Recent advances have highlighted that m6A RNA modification plays an important role in immune response, especially in the initiation and progression of autoimmune diseases. In this review, we summarized the regulatory mechanisms of m6A methylation and its biological functions in the immune system and mainly focused on recent progress in research on the potential role of m6A RNA methylation in the pathogenesis of autoimmune diseases, thus providing possible biomarkers and potential targets for the prevention and treatment of autoimmune diseases.

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Genes & Diseases
Pages 252-267

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Review Status: {{reviewData.commendedNum}} Commended , {{reviewData.revisionRequiredNum}} Revision Required , {{reviewData.notCommendedNum}} Not Commended Under Peer Review

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Cite this article:
Shan Y, Chen W, Li Y. The role of m6A RNA methylation in autoimmune diseases: Novel therapeutic opportunities. Genes & Diseases, 2024, 11(1): 252-267. https://doi.org/10.1016/j.gendis.2023.02.013

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Received: 07 June 2022
Revised: 02 August 2022
Accepted: 08 February 2023
Published: 24 March 2023
© 2023 The Authors.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).