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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.

Life Sciences
|July 20, 2024
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Summary

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.

Keywords:
ApoptosisAutophagyCardiac fibrosisProgrammed cell deathm6A

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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.