NMN protects cisplatin induced AKI via NAD+/SIRT1 pathway

Acute kidney injury (AKI) is a critical public health concern with high morbidity and mortality.Using male mice and HK-2 cells, we found that the NAD? precursor NMN restored renal NAD? levels and activated SIRT1, markedly lowering plasma creatinine and BUN, reducing NGAL and KIM-1 expression, suppressing IL-6/IL-18 and neutrophil infiltration, and attenuating ROS and LDH release. Thus, NMN protects against CIS-AKI via the NAD?–SIRT1 pathway and represents a promising therapeutic strategy. Overall design: RNA-seq profiling of saline-treated control and cisplatin-treated mouse kidneys at 72 h post-injection.