Fig. 9: Schematic illustration.

After I/R stress, Psmb8 expression in cardiomyocytes is downregulated, and causes a reduced interaction between Psmb8 and Drp1 proteins, which enhances Drp1 stability and subsequent excessive mitochondrial fission, leading to reduced ATP level and increased ROS production and apoptosis, all contributing to cardiac I/R injury. Conversely, overexpression of Psmb8 in cardiomyocytes increases Drp1 degradation and improves mitochondrial fission and fusion balance, thereby protecting heart against I/R injury.