Cyclophilin D as a potential therapeutic target of liver ischemia/reperfusion injury by mediating crosstalk between apoptosis and autophagy

Background Liver ischemia/reperfusion (I/R) injury is a complex and multifactorial pathophysiological process. It well recognized that the membrane permeability transition pore (mPTP) opening of mitochondria plays crucial role in cell death after I/R injury. Cyclophilin D (CypD) critical positive regulator mPTP. However, effect CypD on pathogenesis liver whether potential therapeutic target are still unclear. Methods We constructed liver-specific knockout AAV8-peptidyl prolyl isomerase F (PPIF) overexpression mice. Then, 70% model was established mice, with 90 min ischemia 6 h reperfusion. The function detected by level serum glutamic pyruvic transaminase (alanine transaminase) oxaloacetic (aspartate aminotransferase), damage score degree necrosis were measured hematoxylin eosin (H&E) staining tissues. Reactive oxygen species (ROS) staining, apoptosis, autophagy-related molecules used to detect apoptosis autophagy during I/R. Results alleviated dysfunction injury, reducing excessive production ROS, inhibiting autophagy. On contrary, exacerbated I/R-induced damage. Conclusion found downregulation expression through caspase-3/Beclin1 crosstalk; contrast, upregulation aggravated Therefore, interfering seems be promising treatment for