m6A epitranscriptomic and epigenetic crosstalk in cardiac fibrosis

Zhi-Yan Liu ¹, Li-Chan Lin ¹, Zhen-Yu Liu ¹

⁰Department of Anesthesiology and Perioperative Medicine, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, P.R. China.

Molecular Therapy : the Journal of the American Society of Gene Therapy +

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February 5, 2024

View abstract on PubMed

Summary

Cardiac fibrosis, driven by extracellular matrix deposition, is a complex cardiac disease. This review explores the interplay of m6A epitranscriptomics and epigenetics in its progression, offering new therapeutic insights.

Area Of Science

Cardiovascular Research
Molecular Biology
Epigenetics

Background

Cardiac fibrosis, characterized by extracellular matrix deposition, is a key pathological feature of cardiac diseases.
Genetic and epigenetic factors significantly influence cardiac fibrosis progression.
Previous research focused on epigenetic and epitranscriptomic mechanisms in fibrosis.

Purpose Of The Study

To review the intricate interplay between m6A epitranscriptomics and epigenetics in cardiac fibrosis.
To highlight novel therapeutic strategies for cardiac fibrosis treatment.
To provide insights into how these mechanisms regulate pathophysiological processes.

Main Methods

Comprehensive literature review of studies on cardiac fibrosis, m6A epitranscriptomics, and epigenetics.
Analysis of the roles of histone modifications and noncoding RNA in cardiac fibrosis.
Examination of the connection between m6A epitranscriptomics, epigenetics, and cellular processes.

Main Results

The interplay between m6A epitranscriptomics and epigenetics governs key cardiac fibrosis pathways.
This interaction influences mitochondrial dysfunction, oxidative stress, and cell death pathways (apoptosis, pyroptosis, ferroptosis).
Epigenetic and epitranscriptomic factors modulate cell fate switching and differentiation in cardiac fibrosis.

Conclusions

Understanding the m6A epitranscriptomic and epigenetic interplay offers novel therapeutic targets for cardiac fibrosis.
Modulating these mechanisms presents potential solutions for challenging cardiac fibrosis cases.
Further research into this interplay is crucial for advancing cardiac fibrosis treatment.

Keywords:

N6-methyladenosine (m6A) cardiac fibrosis epigenetic epitranscriptomics extracellular matrix