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Cardioprotective signaling to mitochondria Garlid KD; Costa AD; Quinlan CL; Pierre SV; Dos Santos PJ Mol Cell Cardiol 2009[Jun]; 46 (6): 858-66Mitochondria are central players in the pathophysiology of ischemia-reperfusion. Activation of plasma membrane G-coupled receptors or the Na,K-ATPase triggers cytosolic signaling pathways that result in cardioprotection. Our working hypothesis is that the occupied receptors migrate to caveolae, where signaling enzymes are scaffolded into signalosomes that bud off the plasma membrane and migrate to mitochondria. The signalosome-mitochondria interaction then initiates intramitochondrial signaling by opening the mitochondrial ATP-sensitive K(+) channel (mitoK(ATP)). MitoK(ATP) opening causes an increase in ROS production, which activates mitochondrial protein kinase C epsilon (PKCvarepsilon), which inhibits the mitochondrial permeability transition (MPT), thus decreasing cell death. We review the experimental findings that bear on these hypotheses and other modes of protection involving mitochondria.|Animals[MESH]|Humans[MESH]|KATP Channels/metabolism[MESH]|Mitochondria, Heart/metabolism/*physiology[MESH]|Protein Kinase C-epsilon/metabolism[MESH]|Reactive Oxygen Species/metabolism[MESH]|Signal Transduction/*physiology[MESH] |
