The role of N6-methyladenosine (m⁶A) RNA methylation modification in kidney diseases: from mechanism to therapeutic potential

Emerging studies link dysregulated m⁶A machinery to diverse kidney diseases, including acute/chronic kidney injury (WTAP/METTL3/FTO in oxidative stress and fibrosis), and diabetic nephropathy (METTL14/FTO polymorphisms in susceptibility). Mechanistically, m⁶A modulates TGF-β signaling, inflammatory responses, and gene networks underlying disease progression. Despite therapeutic promise, challenges persist in methodological standardization and understanding systemic regulatory roles. Future research should prioritize multi-omics integration, isoform-specific inhibitors, and longitudinal clinical validation. Interdisciplinary efforts to decode m⁶A's multifaceted regulation may advance precision diagnostics and mechanism-based therapies, ultimately improving renal disease management.