Such shifts in mitochondrial dynamics may be prevented or reduced by the activation of sirtuin 1 (SIRT1) or suppression of fission mediator dynamin-related protein 1 (DRP1) as shown by a study conducted on murine models of cisplatin-induced AKI, in which adenosine monophosphate-activated protein kinase (AMPK) agonist 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR), or the antioxidant agent ALCAR, have restored both SIRT3 expression and renal function [21,24]. Here, SIRT3 is linked to acute kidney injury.