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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.
Abstract:
Liver fibrosis is a pathological process caused by a variety of chronic liver diseases. Currently, therapeutic options for liver fibrosis are very limited, highlighting the urgent need to explore new treatment approaches. Epigenetic modifications and epitranscriptomic modifications, as reversible regulatory mechanisms, are involved in the development of liver fibrosis. In recent years, researches in epitranscriptomics and epigenetics have opened new perspectives for understanding the pathogenesis of liver fibrosis. Exploring the epigenetic mechanisms of liver fibrosis may provide valuable insights into the development of new therapies for chronic liver diseases. This review primarily focus on the regulatory mechanisms of N6-methyladenosine (m6A) modification, non-coding RNA, and DNA methylation in organ fibrosis. It discusses the interactions between m6A modification and DNA methylation, as well as between m6A modification and non-coding RNA, providing a reference for understanding the interplay between epitranscriptomics and epigenetics.
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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