Liproxstatin-1 protects the mouse myocardium against ischemia/reperfusion injury by decreasing VDAC1 levels and restoring GPX4 levels - Feng, Yansheng; Madungwe, Ngonidzashe B.; Imam Aliagan, Abdulhafiz D.; Tombo, Nathalie; Bopassa, Jean C. (Biochemical and biophysical research communications, 2019)
Keywords: Animals; Antioxidants - metabolism; calcium; Calcium - metabolism; cardioprotective effect; Cardiotonic Agents - pharmacology; cell viability; Ferroptosis; Ferroptosis - drug effects; Heart - drug effects; Ischemia; Male; Mice; Mice, Inbred C57BL; Mitochondria; Mitochondria, Heart - drug effects; Mitochondria, Heart - metabolism; Mitochondrial Membrane Transport Proteins - drug effects; Mitochondrial Membrane Transport Proteins - metabolism; Mitochondrial Permeability Transition Pore; myocardial infarction; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - pathology; Myocardial Reperfusion Injury - prevention & control; myocardium; Myocardium - metabolism; Myocardium - pathology; oligomerization; permeability; Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism; Quinoxalines - pharmacology; Reactive oxygen species; Reactive Oxygen Species - metabolism; Reperfusion; reperfusion injury; Spiro Compounds - pharmacology; Voltage-Dependent Anion Channel 1 - metabolism; Voltage-Dependent Anion Channel 2 - metabolism; Voltage-Dependent Anion Channels - metabolism; Mitochondria; Reactive oxygen species; IP3R1; Reperfusion; Ischemia; GPX4; ROS; VDAC; Ferroptosis; I/R; mPTP; GRP75