Key result
Pro-survival pathways and regulatory proteins protect against reperfusion injury by inhibiting mPTP opening.
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The mitochondrial permeability transition pore (mPTP) is a non-selective, large-conductance channel that is closed under physiological conditions. Opening of the mPTP, leading to abolition of mitochondrial functions, is a major mechanism of myocyte necrosis by ischaemia/reperfusion, and direct inhibition of mPTP opening by use of pharmacological or genetic manipulations limits infarct size in vivo. Multiple pro-survival signal pathways commonly target the mPTP and inhibit its opening. Although the molecular structure of the mPTP has not been established, recent studies have characterized roles of each mPTP subunit and functions of several proteins directly interacting with the mPTP. This article briefly describes the understanding of mPTP regulation and interaction of the mPTP with four proteins (hexokinase II, glycogen synthase kinase-3β, signal transducer and activator of transcription 3, and sirtuin 3) that are downstream of signal pathways relevant to protection from ischaemia/reperfusion injury.
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Miura et al. (2011) conducted a review in Ischaemia/reperfusion injury. Inhibition of mitochondrial permeability transition pore (mPTP) opening was evaluated on Myocyte necrosis and infarct size. Pro-survival signalling pathways and 4 regulatory proteins (HK II, GSK-3β, STAT3, SIRT3) target the mPTP to inhibit its opening and protect against ischaemia/reperfusion myocyte necrosis.
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