NAT10-mediated ac4C modification of TNFRSF1A promotes acute kidney injury by activating NF-κB pathway

BACKGROUND: C) modification in regulating NF-κB signaling during AKI. METHODS: C modification targets and their effects on RNA stability, translation efficiency, and signaling pathways. RESULTS: C modification enhanced RNA stability and translation efficiency of tumor necrosis factor receptor superfamily member 1A (TNFRSF1A), leading to aberrant NF-κB activation and subsequent inflammatory cascades. CONCLUSIONS: C modification to mitigate NF-κB-dependent pathology.