FTO and diabetic kidney disease: The inflammasome activation axis centers on NLRP3 as a convergent inflammatory mechanism, with WTAP-dependent amplification in diabetic nephropathy promoting IL-1β/IL-18 secretion, FTO suppression inducing PPAR-α hypermethylation in alcohol-induced nephropathy, and IGF2BP1-MIF priming in sepsis-associated AKI (Yu et al., 2021; Lan et al., 2022; Mao et al., 2023).