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Peer-reviewedCC BY 4.0PeerJ

Regulatory roles and molecular mechanisms of N6-methyladenosine (m6A) modification in ischemia-reperfusion injury

  • Di Zhang1
  • Wenjuan An1
  • Xing Zhang1
  • Yuhang Han1
  • Guoxin Zhang2
  • Lingyun Zhang3
  1. 1The First Clinical Medical College of Gansu University of Chinese Medicine, Lanzhou, Gansu, China
  2. 2School of Basic Medical Sciences, Gansu University of Chinese Medicine, Lanzhou, Gansu, China
  3. 3Department of Anesthesiology, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou, Gansu, China
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Abstract

Background: N6-methyladenosine (m6A) represents a prevalent internal epitranscriptomic modification of mRNA that influences post-transcriptional gene regulation. Clinically, ischemia-reperfusion (I/R) injury contributes to tissue damage in acute kidney injury, ischemic stroke, and myocardial infarction, particularly after blood flow is restored.

Methods: We searched Google Scholar, Web of Science, and PubMed for literature published through May 2026. The retrieval focused on articles detailing how m6A effector proteins—specifically writers, erasers, and readers—mediate I/R pathogenesis within hepatic, renal, cardiac, and cerebral tissues.

Results: m6A-associated regulation influences RNA metabolism during I/R injury. Context-dependent changes in m6A regulators and target transcripts are linked to oxidative stress, inflammatory cascades, and specific programmed cell death pathways, including ferroptosis and pyroptosis, across various organ systems.

Conclusion: Profiling these organ-specific m6A molecular networks may inform future research on targeted epitranscriptomic interventions for IRI.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026regulatory,
  title = {{Regulatory roles and molecular mechanisms of N6-methyladenosine (m6A) modification in ischemia-reperfusion injury}},
  author = {Di Zhang and Wenjuan An and Xing Zhang and Yuhang Han and Guoxin Zhang and Lingyun Zhang},
  journal = {PeerJ},
  year = {2026},
  month = nov,
  doi = {10.7717/peerj.21875},
  url = {https://peerj.com/articles/21875},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Regulatory roles and molecular mechanisms of N6-methyladenosine (m6A) modification in ischemia-reperfusion injury
AU  - Di Zhang
AU  - Wenjuan An
AU  - Xing Zhang
AU  - Yuhang Han
AU  - Guoxin Zhang
AU  - Lingyun Zhang
PY  - 2026
DA  - 2026/11/06
JO  - PeerJ
DO  - 10.7717/peerj.21875
UR  - https://peerj.com/articles/21875
AB  - Background: N6-methyladenosine (m6A) represents a prevalent internal epitranscriptomic modification of mRNA that influences post-transcriptional gene regulation. Clinically, ischemia-reperfusion (I/R) injury contributes to tissue damage in acute kidney injury, ischemic stroke, and myocardial infarction, particularly after blood flow is restored.  Methods: We searched Google Scholar, Web of Science, and PubMed for literature published through May 2026. The retrieval focused on articles detailing how m6A effector proteins—specifically writers, erasers, and readers—mediate I/R pathogenesis within hepatic, renal, cardiac, and cerebral tissues.  Results: m6A-associated regulation influences RNA metabolism during I/R injury. Context-dependent changes in m6A regulators and target transcripts are linked to oxidative stress, inflammatory cascades, and specific programmed cell death pathways, including ferroptosis and pyroptosis, across various organ systems.  Conclusion: Profiling these organ-specific m6A molecular networks may inform future research on targeted epitranscriptomic interventions for IRI.
SN  - 2167-8359
ER  -