Acute kidney injury (AKI) is a clinically critical condition with a high mortality rate. Its complex pathophysiological mechanisms remain incompletely understood, and there is a lack of effective targeted therapeutic strategies. In recent years, the role of epigenetic modifications in the initiation and progression of kidney disease has been increasingly clarified. N6-methyladenosine (m6A) is one of the most important and common post-transcriptional modifications among various RNAs, including eukaryotic mRNAs, lncRNAs, and miRNAs. It is dynamically and reversibly regulated by methyltransferases (‘writers’), demethylases (‘erasers’), and binding proteins (‘readers’) to modulate processes such as RNA splicing, export, stability, translation, and degradation. This modification exerts diverse biological effects and is extensively involved in both physiological and pathological pathways. Recently, a growing body of evidence has indicated that m6A modification plays a crucial regulatory role in the development and progression of AKI. Existing studies suggest that m6A modification profoundly influences the fate of renal tubular epithelial cells (TECs) by regulating the expression of genes associated with inflammatory responses and programmed cell death, thereby modulating the severity of AKI and the subsequent renal repair process.
Acute kidney injury (AKI) is a clinically critical condition with a high mortality rate. Its complex pathophysiological mechanisms remain incompletely understood, and there is a lack of effective targeted therapeutic strategies. In recent years, the role of epigenetic modifications in the initiation and progression of kidney disease has been increasingly clarified. N6-methyladenosine (m6A) is one of the most important and common post-transcriptional modifications among various RNAs, including eukaryotic mRNAs, lncRNAs, and miRNAs. It is dynamically and reversibly regulated by methyltransferases (‘writers’), demethylases (‘erasers’), and binding proteins (‘readers’) to modulate processes such as RNA splicing, export, stability, translation, and degradation. This modification exerts diverse biological effects and is extensively involved in both physiological and pathological pathways. Recently, a growing body of evidence has indicated that m6A modification plays a crucial regulatory role in the development and progression of AKI. Existing studies suggest that m6A modification profoundly influences the fate of renal tubular epithelial cells (TECs) by regulating the expression of genes associated with inflammatory responses and programmed cell death, thereby modulating the severity of AKI and the subsequent renal repair process. This review systematically summarizes the latest research advances regarding m6A modification in AKI, elucidates the mechanisms by which it influences the pathogenesis of AKI through various cellular processes, and explores the potential of m6A-targeted therapies for treating AKI, thereby providing insights into the regulatory networks of m6A modification in AKI and the epigenetic regulation of transcription in this condition.