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m 6 A modification in non-coding RNAs: Mechanisms and potential therapeutic implications in fibrosis.

Yutong ZhouNi JianCanhua JiangJie Wang
Published in: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie (2024)
N6-methyladenosine (m 6 A) 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. m 6 A 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 m 6 A regulators, including writers, erasers, and readers, have been reported to modify the ncRNAs involved in fibrogenesis. NcRNAs affect fibrosis progression by targeting m 6 A regulators. The interactions between m 6 A and ncRNAs can influence multiple cellular life activities. In this review, we discuss the impact of the interaction between m 6 A modifications and ncRNAs on the pathological mechanisms of fibrosis, revealing the possibility of these interactions as diagnostic markers and therapeutic targets in fibrosis.
Keyphrases
  • long non coding rna
  • transcription factor
  • liver fibrosis
  • poor prognosis
  • dna methylation
  • stem cells
  • bone marrow