PINK1-mediated mitochondrial autophagy protects lens epithelial cells by reducing ROS and apoptosis

Cataracts are one of the primary causes of blindness worldwide; however, their pathogenesis remains unclear. Oxidative stress and apoptosis are two dominant inducers in the progression of cataracts; however, little is known about the specific mechanisms associated with mitophagy. This study aimed to investigate the role of PTEN-induced putative kinase 1(PINK1)-mediated mitophagy in cataract development. Initially, we induced a rat cataract model using sodium selenite and observed the upregulated expression of PINK1 and other autophagy-related proteins within lens epithelial cells, accompanied by apoptosis. Furthermore, the survival rate of human lens epithelial cells was significantly reduced by H₂O₂ treatment. However, PINK1 overexpression reduced ROS levels, allowing cells to survive. This reduction in reactive oxygen species (ROS) levels led to a decrease in cleaved caspase-3 and Bcl-2-associated X protein (Bax) expression and an increase in B-cell lymphoma 2 (Bcl-2) levels. In summary, PINK1 maintains mitochondrial functional stability and inhibits apoptosis by activating mitophagy, thus potentially playing a crucial protective role in cataract pathogenesis.