N(6)-methyladenosine modification: A vital role of programmed cell death in myocardial ischemia/reperfusion injury

Jian Wang1, Yanyan Li2, Song Zhang1

  • 1Department of Cardiology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China.

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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