Furthermore, Sirt3‐knockout mice and Sirt3‐overexpressing HK‐2 cells were used to construct a septic model and further observe the changes in mitochondrial function and dynamics, as well as the activity levels of upstream related molecules, to evaluate the role of Sirt3 in mitochondrial injury in TECs in septic AKI and the mechanism. The gene discussed is SIRT3; the disease is acute kidney injury.