DEX pre-treatment can reduce p-CaMKII levels and alleviate ROS-mediated Ca2+ overload, inhibiting phosphorylation of Drp1 Ser616 and its translocation to mitochondria caused by CaMKII activation, thereby inhibiting mitochondrial division and protecting AKI caused by sepsis while Atip reversed this down-regulation. This evidence concerns the gene MTUS1 and Sepsis.