Diabetic kidney disease (DKD) is a leading cause of end-stage renal disease, characterized by pathological changes such as decreased glomerular filtration rate and proteinuria. As a key component of the glomerular filtration barrier, podocyte injury is closely associated with the progression of DKD. Recent studies have revealed that mitochondrial dysfunction plays a central role in podocyte injury in DKD, primarily manifested as enhanced mitochondrial oxidative stress, defective autophagy, and fission/fusion imbalance. These alterations lead to excessive production of reactive oxygen species and inflammatory factors, thereby accelerating podocyte apoptosis. Meanwhile, multiple signaling pathways-including NOX4/TRPC6, TGF-β1/SMAD, AMPK/PGC-1α, and PINK1/Parkin-can intervene in mitochondrial damage-induced podocyte apoptosis, while dysregulation of genes related to podocyte mitochondrial function exacerbates DKD. This article systematically reviews the critical roles of relevant signaling pathways and mitochondrial DNA in mediating podocyte mitochondrial injury during DKD progression, aiming to provide new theoretical foundations and therapeutic targets for DKD prevention and treatment. Additionally, it explores the potential of traditional Chinese medicine targeting podocyte mitochondria as a strategy to delay DKD progression.