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

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.