Mechanistic Study of the Pink1/Parkin Signaling Pathway in Mitochondrial Dysfunction and Podocyte Injury

PTEN-Induced Putative Kinase 1 (Pink1) is a key regulatory protein in mitochondrial autophagy: upon mitochondrial damage, Pink1 selectively binds to the mitochondrial outer membrane, thereby recruiting and phosphorylating Parkin. However, the mechanism by which the Pink1/Parkin signaling pathway functions in podocytes remains unclear, and this study aimed to investigate the role of this pathway in mitochondrial dysfunction associated with glomerular podocyte injury. For this purpose, flow cytometry was used to detect podocyte apoptosis rate; transmission electron microscopy was employed to observe the quantity and morphological changes of podocyte mitochondrial autophagosomes; and reverse transcription-polymerase chain reaction (RT-PCR) and western blot were performed to quantify the mRNA and protein expression levels of Pink1, Parkin, and LC3-II, respectively. The results showed that compared with the Control and Pink1 groups, the PAN group exhibited a significantly increased podocyte apoptosis rate; in the Pink1 group, mitochondria gradually became swollen and rounded, with disordered arrangement. These findings confirmed that PAN can induce podocyte injury and that this process is associated with the Pink1/Parkin pathway. In conclusion, the Pink1/Parkin signaling pathway plays a crucial role in mitochondrial dysfunction during glomerular podocyte injury, and these results provide a new perspective for the potential clinical application of the Pink1/Parkin signaling pathway in podocyte injury and future related research.