N(6)-methyladenosine modification: A vital role of programmed cell death in myocardial ischemia/reperfusion injury
Related Experiment Video
Updated: Aug 31, 2025

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Jian Wang1, Yanyan Li2, Song Zhang1
1Department of Cardiology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China.
Abstract:
N(6)-methyladenosine (m6A) modification is closely associated with myocardial ischemia/reperfusion injury (MIRI). As the most common modification among RNA modifications, the reversible m6A modification is processed by methylase ("writers") and demethylase ("erasers"). The biological effects of RNA modified by m6A are regulated under the corresponding RNA binding proteins (RBPs) ("readers"). m6A modification regulates the whole process of RNA, including transcription, processing, splicing, nuclear export, stability, degradation, and translation. Programmed cell death (PCD) is a regulated mechanism that maintains the internal environment's stability. PCD plays an essential role in MIRI, including apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis. However, the relationship between PCD modified with m6A and MIRI is still not clear. This review summarizes the regulators of m6A modification and their bioeffects on PCD in MIRI.
Insights
N(6)-methyladenosine (m6A) RNA modification influences myocardial ischemia/reperfusion injury (MIRI) by regulating programmed cell death (PCD). This review explores m6A regulators and their impact on PCD in MIRI.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Epigenetics
Background:
- N(6)-methyladenosine (m6A) is the most prevalent RNA modification, impacting RNA metabolism.
- m6A modification is dynamically regulated by
- writers
- erasers
- and
- readers
- (RNA binding proteins).
- Programmed cell death (PCD) pathways, including apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis, are crucial in myocardial ischemia/reperfusion injury (MIRI).
Purpose of the Study:
- To review the regulatory mechanisms of m6A modification.
- To elucidate the role of m6A modification in various PCD pathways.
- To understand the intricate relationship between m6A-modified PCD and MIRI.
Main Methods:
- Literature review of studies on m6A modification, PCD, and MIRI.
- Analysis of the functions of m6A regulators (writers, erasers, readers).
- Synthesis of current knowledge on m6A's impact on different PCD types in the context of MIRI.
Main Results:
- m6A modification influences multiple stages of RNA processing and function.
- Specific m6A regulators have been implicated in modulating apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis.
- Evidence suggests a significant role for m6A-mediated PCD in the pathogenesis of MIRI.
Conclusions:
- m6A modification is a key epigenetic regulator in MIRI.
- Targeting m6A pathways offers potential therapeutic strategies for MIRI.
- Further research is needed to fully understand the m6A-PCD interplay in MIRI.
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