m6A modification in non-coding RNAs: Mechanisms and potential therapeutic implications in fibrosis
- PMID: 39191030
- DOI: 10.1016/j.biopha.2024.117331
m6A modification in non-coding RNAs: Mechanisms and potential therapeutic implications in fibrosis
Abstract
N6-methyladenosine (m6A) is one of the most prevalent and reversible forms of RNA methylation, with increasing evidence indicating its critical role in numerous physiological and pathological processes. m6A catalyzes messenger RNA(mRNA) as well as regulatory non-coding RNAs (ncRNAs), such as microRNAs, long non-coding RNAs, and circular RNAs. This modification modulates ncRNA fate and cell functions in various bioprocesses, including ncRNA splicing, maturity, export, and stability. Key m6A regulators, including writers, erasers, and readers, have been reported to modify the ncRNAs involved in fibrogenesis. NcRNAs affect fibrosis progression by targeting m6A regulators. The interactions between m6A and ncRNAs can influence multiple cellular life activities. In this review, we discuss the impact of the interaction between m6A modifications and ncRNAs on the pathological mechanisms of fibrosis, revealing the possibility of these interactions as diagnostic markers and therapeutic targets in fibrosis.
Keywords: Fibrosis; M(6)A RNA methylation; Noncoding RNAs.
Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.
Conflict of interest statement
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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