AQP5 deficiency promotes the senescence of lens epithelial cells through mitochondrial dysfunction

Cataract is lens opacity, which is a common blinding eye disease worldwide. Aquaporin 5 (AQP5) is expressed in the human and mouse lenses. This study aimed to investigate the underlying mechanisms of AQP5 in the senescence of lens epithelial cells (LECs). Primary LECs were isolated and cultured from Aqp5+/+ and Aqp5−/− mice. Western blot or immunofluorescence staining of p16, Ki67, MitoSOX, JC-1 and phalloidin was used in the experiments to evaluate the changes in the primary LECs. The primary Aqp5−/− LECs showed increased p16 expression and mitochondrial reactive oxygen species, decreased mitochondrial membrane potential and activity, and cytoskeletal disorders. When the cells were pretreated with Mito-TEMPO, the Aqp5−/− mice showed decreased p16 expression, reduced mitochondrial dysfunction and cytoskeletal disorders. Our results revealed that AQP5 deficiency promotes the senescence of primary LECs through mitochondrial dysfunction. This provides a new perspective for the treatment of cataracts by regulating AQP5 expression. •AQP5 deficiency promotes the senescence of lens epithelial cells.•AQP5 deficiency results in mitochondrial dysfunction in lens epithelial cells.•The involvement of AQP5 in treating age-related cataracts offers a novel therapeutic approach for ocular disorders.