m6A epitranscriptomic and epigenetic crosstalk in liver fibrosis: Special emphasis on DNA methylation and non-coding

Qi-Qi Dong1, Yang Yang2, Hui Tao3

  • 1Department of Clinical Pharmacology, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, China; School of Pharmacy, Anhui Medical University, Hefei 230032, China.

Cellular Signalling
|July 18, 2024
PubMed

Insights

Liver fibrosis treatments are limited. This review explores how N6-methyladenosine (m6A) modification, non-coding RNA, and DNA methylation influence liver fibrosis, offering new therapeutic insights.

Area of Science:

  • Molecular biology
  • Hepatology
  • Epigenetics

Background:

  • Liver fibrosis is a significant pathological process in chronic liver diseases with limited therapeutic options.
  • Epigenetic and epitranscriptomic modifications are increasingly recognized as key players in liver fibrosis development.
  • Understanding these reversible regulatory mechanisms is crucial for developing novel treatments.

Purpose of the Study:

  • To review the regulatory mechanisms of N6-methyladenosine (m6A) modification, non-coding RNA, and DNA methylation in organ fibrosis.
  • To explore the interplay between epitranscriptomics and epigenetics in the context of liver fibrosis.
  • To provide a reference for understanding the pathogenesis and potential therapeutic targets in chronic liver diseases.

Main Methods:

  • Literature review focusing on epigenetic and epitranscriptomic modifications in liver fibrosis.
  • Analysis of regulatory mechanisms involving N6-methyladenosine (m6A) modification, non-coding RNA, and DNA methylation.
  • Discussion of the interactions between m6A modification and DNA methylation, and between m6A modification and non-coding RNA.

Main Results:

  • N6-methyladenosine (m6A) modification, non-coding RNA, and DNA methylation are integral to the development of liver fibrosis.
  • Complex interactions exist between m6A modification, DNA methylation, and non-coding RNA in fibrogenesis.
  • These epigenetic and epitranscriptomic mechanisms offer potential avenues for therapeutic intervention.

Conclusions:

  • Epigenetic and epitranscriptomic modifications, particularly m6A, non-coding RNA, and DNA methylation, are critical in liver fibrosis.
  • Understanding the intricate interplay between these mechanisms provides valuable insights into chronic liver disease pathogenesis.
  • Targeting these epigenetic regulators may lead to the development of innovative therapies for liver fibrosis.

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