Chiba T, Peasley KD, Cargill KR, et al. - Researchers investigated the role of sirtuin 5 (Sirt5) in regulating kidney energy metabolism. Male Sirt5-deficient mice (either +/− or −/−) and wild-type controls, as well as isolated proximal tubule cells, were subjected to 2 different AKI models (ischemia-induced or cisplatin-induced AKI). Using standard techniques, kidney function and injury were evaluated. They measured fatty acid oxidation by the catabolism of ¹⁴C-labeled palmitate to ¹⁴CO₂. High expression of Sirt5 in proximal tubular epithelial cells was found. In proximal tubular epithelial cells, the regulation of the balance of mitochondrial vs peroxisomal fatty acid oxidation by Sirt5 to protect against injury in AKI was seen. This new mechanism might be leveraged for developing AKI treatments.