Key result
Opening of mitochondrial K(ATP) channels is linked to protection against ischemia-reperfusion injury and apoptosis, though structural information and clear physiological roles remain to be fully defined.
This review highlights the physiological role of mitochondrial K(ATP) channels in cardioprotection against ischemia-reperfusion injury.
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Mitochondrial K(ATP) channels merit mechanistic study for ischemia-reperfusion protection; leaves open structural details and clinical translation.
Twenty years after the discovery of sarcolemmal ATP-sensitive K+ channels and 12 years after the discovery of mitochondrial K(ATP) (mitoK(ATP)) channels, progress has been remarkable, but many questions remain. In the case of the former, detailed structural information is available, and it is well accepted that the channel couples bioenergetics to cellular electrical excitability; however, in the heart, a clear physiological or pathophysiological role has yet to be defined. For mitoK(ATP), structural information is lacking, but there is abundant evidence linking the opening of the channel to protection against ischemia-reperfusion injury or apoptosis. This review updates recent progress in understanding the physiological role of mitoK(ATP) and highlights outstanding questions and controversies, with the intent of stimulating additional investigation on this topic.
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Brian O’Rourke (2004) conducted a review in Ischemia-reperfusion injury. Mitochondrial K(ATP) channels was evaluated. Opening of mitochondrial K(ATP) channels is linked to protection against ischemia-reperfusion injury and apoptosis, though structural information and clear physiological roles remain to be fully defined.
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