Table 1.
Expression patterns and functional roles of m6A regulators in various models of AKI.
| AKI model | Cell type | m6A regulator | Expression | Target | Key findings | Reference |
|---|---|---|---|---|---|---|
| Cisplatin, LPS, and I/R-induced AKI | HK-2, mTECs | METTL3, IGF2BP2 | Upregulated | TAB3 | METTL3 promotes renal inflammation and programmed cell death | (50) |
| Lead acetate-induced AKI | HK2 | METTL3 | Upregulated | HKDC1 | METTL3 promotes renal injury and inflammation | (63) |
| Ischemic, septic, and vancomycin-induced AKI | BUMPT | METTL3 | Upregulated | mmu-lncRNA 121686/hsa-lncRNA 520657 | METTL3 promotes AKI via the lncRNA 121686/miR-328-5p/HtrA3 axis | (64) |
| CLP- induced AK | RAW264.7 | FTO | Downregulated | MMP-9 | FTO reduces M1 macrophage polarization and attenuates LPS-induced inflammation | (65) |
| CLP- induced AKI | HK2 | IGF2BP1 | Upregulated | E2F1 | IGF2BP1 targets the MIF component of NLRP3 inflammasome, acting as a potent pyroptosis inducer in septic AKI | (61) |
| CLP- induced AKI | HK-2 | METTL3, YTHDF1 | Upregulated | MDM2 | METTL3-mediated m6A modification regulates the MDM2-p53-LMNB1 axis, stimulating mitochondrial damage and ferroptosis in TECs | (66) |
| CLP- induced AKI | HK-2 | METTL14 | Downregulated | HMOX1 | METTL14 inhibits ferroptosis and protects against AKI via m6A-dependent regulation of HMOX1 | (54) |
| CLP- induced AKI | HK2 | HNRNPC | Upregulated | NF-κB p65 | HNRNPC-mediated m6A drives tubular dysfunction in sepsis-induced AKI | (67) |
| CLP- induced AKI | Mouse microvascular pericytes | MTHFD2 | Upregulated | LOX | MTHFD2 promotes LOX expression in an m6A-dependent manner, mediating AKI progression | (68) |
| LPS- induced AKI | TCMK-1 | METTL3 | Upregulated | MALAT1 | METTL3 promotes inflammatory cytokine release and pyroptosis in AKI by enhancing m6A modification of MALAT1 | (69) |
| LPS- induced AKI | TCMK-1 | RBM15 and IGF2BP1 | Upregulated | CRBN | RBM15 increases CRBN m6A modification and promotes its expression in an IGF2BP1-dependent manner, enhancing pyroptosis in TECs | (70) |
| LPS- induced AKI | HK-2 | WTAP | Upregulated | LMNB1 | WTAP-mediated m6A promotes LPS-induced inflammation, mitochondrial damage, and ferroptosis by regulating LMNB1 expression and activating NF-κB and JAK2/STAT3 pathways | (71) |
| LPS- induced AKI | TCMK-1 | METTL14 | Upregulated | LPCAT3 | METTL14 promotes ferroptosis in septic AKI by increasing m6A methylation of LPCAT3 | (52) |
| LPS- induced AKI | HK2 | FTO | Downregulated | SNHG14 | FTO regulates LPS-induced cell viability, apoptosis, and autophagy via the SNHG14/miR-373-3p/ATG7 interaction network | (56) |
| LPS- induced AKI | HK-2 | ALKBH5 | Upregulated | pri-miR-205 | ALKBH5 suppresses miR-205-5p expression by removing m6A modification, thereby upregulating DDX5 and promoting EMT and the AKI-to-CKD transition | (72) |
| I/R- induced AKI | mRTEC | ALKBH5 | Upregulated | CCL28 | ALKBH5 inhibits renal Treg recruitment, increases macrophage and neutrophil infiltration, and promotes inflammation | (58) |
| I/R- induced AKI | Mouse TECs | METTL14, IGF2BP2 | Downregulated | PPARγ | METTL14 regulates PPARγ m6A methylation in an IGF2BP2-dependent manner, playing a crucial role in alleviating renal I/R injury and TEC ferroptosis | (55) |
| I/R- induced AKI | HK-2, TCMK-1 | METTL3 | Upregulated | miR-374b-5p | METTL3 promotes renal I/R injury by regulating the miR-374b-5p/SRSF7 axis | (73) |
| I/R- induced AKI | HK2 | METTL3 and IGF2BP2 | Upregulated | TIFA | METTL3 enhances TIFA mRNA stability in an IGF2BP2-dependent manner, thereby promoting pyroptosis | (74) |
| I/R- induced AKI | HK-2 | FTO | Downregulated | Ambra1 | FTO promotes autophagy by upregulating the Ambra1/ULK1 signaling pathway, thereby inhibiting oxidative stress and renal injury | (57) |
| Cisplatin and I/R-induced AKI | HK2 | YTHDF1 | Upregulated | SHPK1 | YTHDF1 alleviates AKI by protecting m6A-methylated mRNAs within renal tubular stress granules | (60) |
| Cisplatin - induced AKI | HK-2 | METTL14、IGF2BP3 | Upregulated | ERFE | METTL14 stabilizes ERFE mRNA through IGF2BP3-dependent m6A modification, promoting ferroptosis in cisplatin-induced AKI | (53) |
| Cisplatin - induced AKI | HK-2 | ALKBH5 | Upregulated | — | ALKBH5 promotes cisplatin-induced AKI and ferroptosis | (59) |
| Cisplatin - induced AKI | HK-2 | METTL3 | Upregulated | SREBP1c | METTL3-mediated upregulation of SREBP1c disrupts mitochondrial energy metabolism by transcriptionally repressing YME1L1, promoting AKI and its progression to CKD | (75) |
| Cisplatin - induced AKI | HK-2 | IGF2BP3 | Downregulated | NCBP1 | IGF2BP3 inhibits TEC senescence and is involved in cisplatin-induced AKI and its progression to CKD | (62) |
| Cisplatin - induced AKI | HK2 | ZC3H13 | Upregulated | NABP1 | ZC3H13 knockdown alleviates G2/M cell cycle arrest, apoptosis, and renal injury by affecting NABP1 expression | (51) |
| Cisplatin - induced AKI | HK2 | , FTO | Downregulated | p53 | Reduced renal FTO expression increases RNA m6A levels and exacerbates kidney injury in cisplatin-induced AKI | (76) |
| TNF-α-induced AKI | HK-2 | FTO | — | AQP3 | FTO alleviates TNF-α-induced TEC injury by targeting AQP3 in an m6A-dependent manner | (77) |
| Folic acid-induced AKI | TCMK-1 | METTL3 | Upregulated | ASC | METTL3 promotes inflammatory cytokine release and pyroptosis | (78) |
| Folic acid-induced AKI | TCMK-1 | METTL3,GF2BP3 | Upregulated | Hmox1/HO-1 | METTL3 mediates m6A modification of HO-1 mRNA and maintains its stability in an IGF2BP3-dependent manner, thereby promoting ferroptosis | (79) |