Mitochondrial dysfunction is recognized as a primary characteristic and key process in AKI,[14] serving both as an initiator and contributor.[4] In particular, mitochondrial proteins, such as Aldehyde dehydrogenase family 1 member L2 (ALDH1L2),[15] Sirtuin 3 (Sirt3),[16] and Sirtuin 5 (Sirt5),[17] play crucial roles in maintaining mitochondrial function, thereby preventing or ameliorating AKI and its progression to CKD. This evidence concerns the gene SIRT3 and acute kidney injury.