La desubiquitinasa YOD1 en células epiteliales tubulares renales promueve la enfermedad renal diabética al estabilizar KEAP1

stimulation, thus increasing oxidative stress. Similarly, the ROS scavenger N-acetylcysteine (NAC) can alleviate oxidative stress injury to some extent by reducing ROS levels in RTECs. Finally, we confirmed that the YOD1 pharmacological inhibitor G5 has therapeutic effects on kidney injury in diabetic mice. Our findings demonstrate that the YOD1-KEAP1 axis mediates oxidative stress injury in RTECs and highlight that targeting YOD1 represents a © 2026. The Author(s) under exclusive licence to The Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society.