Consistent with AKF-PD's broad antifibrotic actions and the important contributions of mitochondrial dysfunction to renal fibrosis, our recent evidence demonstrated that AKF-PD can reduce mitochondrial damage by inhibiting mitochondrial oxidative stress in the folic acid-induced renal fibrosis model, where downregulation of NADPH oxidase 4 (NOX4) expression may play a role [16]. Here, NOX4 is linked to renal fibrosis.