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. 2026 Jul 13;17:1864973. doi: 10.3389/fimmu.2026.1864973

Figure 2.

Diagram illustrating the roles of m6A RNA modification in acute kidney injury. Different mRNAs, such as TAB3, HKDC1, PPARγ, MMP-9, and CCL28, undergo modifications by writers (METTL3, METTL14), erasers (FTO, ALKBH5), and readers (IGF2BP2), influencing translation efficiency and promoting or inhibiting inflammation, ultimately contributing to acute kidney injury. A kidney graphic highlights inflammation and affected regions. A legend identifies m6A modification, writer, eraser, reader, and promotion or inhibition arrows.

Molecular mechanisms of m6A modification in regulating inflammation during AKI. This schematic illustrates how m6A writers (METTL3 and METTL14) and erasers (FTO and ALKBH5) modulate inflammatory pathways to influence AKI progression. METTL3 and METTL14 mediate m6A methylation of downstream target genes, enhancing their expression and thereby activating inflammatory signaling cascades that drive AKI progression. In contrast, FTO and ALKBH5 remove m6A modifications from target transcripts and regulate immune cell activity, thereby attenuating or modulating the inflammatory response during AKI progression.