METTL3 and chronic kidney disease: The TGF-β/m6A axis establishes a bidirectional relationship where TGF-β signaling induces METTL3 expression in acute kidney injury (enhancing pro-fibrotic transcript modification), perpetuates CKD progression through Smad3 phosphorylation, exacerbates diabetic podocyte injury via TIMP2/Notch activation, and drives obstructive nephropathy EMT through C/EBPβ-mediated mechanisms (Wang et al., 2022; Jung et al., 2024; Yang et al., 2024c).