Dipyridamole Confers Renoprotection Against Rhabdomyolysis-Induced Acute Kidney Injury via Modulation of Oxidative Stress, the PKC/ET-1/PI3K/AKT Signaling Axis, and Apoptosis

Background

Rhabdomyolysis (RM)-induced acute kidney injury (RIAKI) is a common clinical complication with an increasing incidence. Despite optimal care, the mortality rate is almost 15% due to limited pharmacological interventions. Dipyridamole (DPM), a non-selective phosphodiesterase inhibitor, possesses antioxidant, anti-inflammatory, and antiproliferative properties. This study aimed to investigate the protective effect of DPM against glycerol (GLY)-induced RIAKI, focusing on key AKI-related signaling pathways, including the protein kinase C (PKC)/endothelin-1 (ET-1)/phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mitogen-activated protein kinase (MAPK) cascade, and apoptotic and proliferative responses.