2015
DOI: 10.1111/bph.13013
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Role of the MPTP in conditioning the heart – translatability and mechanism

Abstract: Mitochondria have long been known to be the gatekeepers of cell fate. This is particularly so in the response to acute ischaemia‐reperfusion injury (IRI). Following an acute episode of sustained myocardial ischaemia, the opening of the mitochondrial permeability transition pore (MPTP) in the first few minutes of reperfusion, mediates cell death. Preventing MPTP opening at the onset of reperfusion using either pharmacological inhibitors [such as cyclosporin A (CsA) ] or genetic ablation has been reported to red… Show more

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Cited by 65 publications
(61 citation statements)
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“…Critical target of IPC is the mPTP whose excessive opening in the first few minutes of reperfusion induces cardiomyocyte death. Key inducers of mPTP opening are ATP depletion, excessive generation of ROS, mitochondrial Ca 2+ overload and changes of intracellular pH 32 . Therefore, preserving ATP levels, attenuation of oxidative stress and mitochondrial Ca 2+ overload, and delayed correction of ischemia-induced intracellular acidosis are integrated in the IPC-mediated inhibition of mPTP opening 33,34 .…”
Section: Discussionmentioning
confidence: 99%
“…Critical target of IPC is the mPTP whose excessive opening in the first few minutes of reperfusion induces cardiomyocyte death. Key inducers of mPTP opening are ATP depletion, excessive generation of ROS, mitochondrial Ca 2+ overload and changes of intracellular pH 32 . Therefore, preserving ATP levels, attenuation of oxidative stress and mitochondrial Ca 2+ overload, and delayed correction of ischemia-induced intracellular acidosis are integrated in the IPC-mediated inhibition of mPTP opening 33,34 .…”
Section: Discussionmentioning
confidence: 99%
“…Although the mechanisms underlying ischemic post-conditioning are not fully elucidated, it has been shown to be associated with inhibition of mPTP opening. This may be partially explained by maintenance of an acid pH (inhibitory for mPTP opening) for longer during the early stages of reperfusion, but other signalling pathways are also thought to be involved [44,55]. There are no published data to show that reduced ROS production during the early stages of reperfusion post-conditioning is the mechanism by which it inhibits mPTP.…”
Section: Discussionmentioning
confidence: 99%
“…For example, evidence shows that PKG can protect cells from IR injury by activating signaling cascades that delay mPTP opening [60][61][62].…”
Section: Discussionmentioning
confidence: 99%