Neutrophil‐Mimetic Nanoscavengers Target the Inflammatory Microenvironment to Eliminate NETs/ROS and Immunomodulate cGAS‐STING Signaling in Septic AKI

nanozymes catalytically scavenge ROS and the loaded DNase-1 enzymatically degrades NETs-derived extracellular DNA, thereby suppressing the cGAS-STING pathway and skewing macrophage polarization toward an M2 reparative phenotype. In a murine model of LPS-induced SAKI, MD@NM treatment facilitated robust renal targeting, attenuated neutrophilic infiltration, resolved cytokine storm, and ameliorated structural kidney damage. Collectively, this biomimetic platform represents a novel strategy for precision immunomodulation and multi-mechanistic therapy against SAKI by integrating antioxidative, NETs-scavenging, and anti-inflammatory functions into a single nanotherapeutic agent.