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Updated: Jun 20, 2025
Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
m6A control programmed cell death in cardiac fibrosis
Zhen-Yu Liu1, Qing-Ye You2, Zhi-Yan Liu1
1Department of Anesthesiology and Perioperative Medicine, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, PR China.
Abstract:
N6-methyladenosine (m6A) modification is closely related to cardiac fibrosis. As the most common and abundant form of mRNA modification in eukaryotes, m6A is deposited by methylases ("writers"), recognized and effected by RNA-binding proteins ("readers"), and removed by demethylases ("erasers"), achieving highly dynamic reversibility. m6A modification is involved in regulating the entire biological process of target RNA, including transcription, processing and splicing, export from the nucleus to the cytoplasm, and enhancement or reduction of stability and translation. Programmed cell death (PCD) comprises many forms and pathways, with apoptosis and autophagy being the most common. Other forms include pyroptosis, ferroptosis, necroptosis, mitochondrial permeability transition (MPT)-dependent necrosis, and parthanatos. In recent years, increasing evidence suggests that m6A modification can mediate PCD, affecting cardiac fibrosis. Since the correlation between some PCD types and m6A modification is not yet clear, this article mainly introduces the relationship between four common PCD types (apoptosis, autophagy, pyroptosis, and ferroptosis) and m6A modification, as well as their role and influence in cardiac fibrosis.
Insights
N6-methyladenosine (m6A) modification influences cardiac fibrosis by regulating programmed cell death (PCD). This review explores how m6A impacts apoptosis, autophagy, pyroptosis, and ferroptosis in cardiac fibrosis.
Area of Science:
- Molecular Biology
- Cardiovascular Biology
- Epigenetics
Background:
- N6-methyladenosine (m6A) is the most prevalent mRNA modification in eukaryotes.
- m6A regulates RNA processing, stability, and translation.
- m6A modification is increasingly linked to programmed cell death (PCD) pathways.
Purpose of the Study:
- To elucidate the role of m6A modification in mediating PCD.
- To investigate the influence of m6A-mediated PCD on cardiac fibrosis.
- To review the relationship between m6A and four common PCD types: apoptosis, autophagy, pyroptosis, and ferroptosis.
Main Methods:
- Literature review of studies on m6A modification, PCD, and cardiac fibrosis.
- Analysis of existing evidence connecting m6A regulators (writers, readers, erasers) with PCD pathways.
- Synthesis of findings on the impact of m6A-mediated PCD on the development and progression of cardiac fibrosis.
Main Results:
- m6A modification dynamically regulates gene expression involved in PCD.
- Specific PCD pathways, including apoptosis, autophagy, pyroptosis, and ferroptosis, are modulated by m6A.
- Dysregulation of m6A-mediated PCD contributes to the pathogenesis of cardiac fibrosis.
Conclusions:
- m6A modification plays a critical role in orchestrating programmed cell death.
- Targeting m6A pathways offers potential therapeutic strategies for cardiac fibrosis.
- Further research is needed to fully understand the intricate interplay between m6A and various PCD forms in cardiovascular disease.
