Description
Cisplatin-induced acute kidney injury (AKI) is one of the most common and severe side effects and can prevent the use of this important agent. Unfortunately, preventive or therapeutic tools to address cisplatin-induced AKI are lacking. Interestingly, in the last decades a row of preconditioning strategies that employ the activation of cellular stress resistance pathways have been shown to be promising approaches to protect from organ injury in rodent models. Here, we characterized both the protective potential and the underlying molecular patterns of two strategies caloric restriction and hypoxic preconditioning in mice treated with cisplatin.
Overall Design
mRNA profiles of mouse kidney after cisplatin injection with preconditioning baseline, caloric restriction and hypoxia.
Curator
hy_li