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lüll Cardioprotection by metabolic shut-down and gradual wake-up Burwell LS; Nadtochiy SM; Brookes PSJ Mol Cell Cardiol 2009[Jun]; 46 (6): 804-10Mitochondria play a critical role in cardiac function, and are also increasingly recognized as end effectors for various cardioprotective signaling pathways. Mitochondria use oxygen as a substrate, so by default their respiration is inhibited during hypoxia/ischemia. However, at reperfusion a surge of oxygen and metabolic substrates into the cell is thought to lead to rapid reestablishment of respiration, a burst of reactive oxygen species (ROS) generation and mitochondrial Ca(2+) overload. Subsequently these events precipitate opening of the mitochondrial permeability transition (PT) pore, which leads to myocardial cell death and dysfunction. Given that mitochondrial respiration is already inhibited during hypoxia/ischemia, it is somewhat surprising that many respiratory inhibitors can improve recovery from ischemia-reperfusion (IR) injury. In addition ischemic preconditioning (IPC), in which short non-lethal cycles of IR can protect against subsequent prolonged IR injury, is known to lead to endogenous inhibition of several respiratory complexes and glycolysis. This has led to a hypothesis that the wash-out of inhibitors or reversal of endogenous inhibition at reperfusion may afford protection by facilitating a more gradual wake-up of mitochondrial function, thereby avoiding a burst of ROS and Ca(2+) overload. This paper will review the evidence in support of this hypothesis, with a focus on inhibition of each of the mitochondrial respiratory complexes.|Electron Transport Complex I/metabolism/physiology[MESH]|Electron Transport Complex II/metabolism/physiology[MESH]|Electron Transport Complex III/metabolism/physiology[MESH]|Electron Transport Complex IV/metabolism/physiology[MESH]|Glycolysis/physiology[MESH]|Ischemic Preconditioning, Myocardial[MESH]|Mitochondria/metabolism/physiology[MESH]|Models, Biological[MESH]|Myocardial Reperfusion Injury/*metabolism/*physiopathology/prevention & control[MESH]|Nitric Oxide/metabolism/physiology[MESH] |