CASK mediates methylglyoxal-induced mitochondria-associated cell death in retinal Müller cells through modulating the ROS-p38-SOCE signalling pathway and antioxidant enzymes

accumulation and apoptosis. Transcriptomic analysis revealed that CASK silencing upregulated genes involved in mitochondrial respiration and oxidative phosphorylation, particularly complexes I and V. Collectively, these findings demonstrate that CASK promotes MGO-induced apoptosis through kinase-independent disruption of mitochondrial and antioxidant defenses, and kinase-dependent activation of SOCE, identifying CASK as a potential therapeutic target in DR.