Inhibiting mitochondrial permeability transition pore opening at reperfusion protects against ischaemia-reperfusion injury.

@article{Hausenloy2003InhibitingMP,
  title={Inhibiting mitochondrial permeability transition pore opening at reperfusion protects against ischaemia-reperfusion injury.},
  author={Derek J. Hausenloy and Michael R. Duchen and Derek M. Yellon},
  journal={Cardiovascular research},
  year={2003},
  volume={60 3},
  pages={
          617-25
        }
}
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445 Citations
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Background Citations
173
Methods Citations
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445 Citations

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TLDR
Interventions which target and inhibit mPTP opening, at the time of reperfusion, may improve morbidity and mortality from coronary artery disease, in the clinical settings of ischaemia-reperfusion injury such as thrombolysis following an acute myocardial infarction, heart surgery and percutaneous transluminal coronary angioplasty.
EVIDENCE THAT HYDROXYSAFFLOR YELLOW A PROTECTS THE HEART AGAINST ISCHAEMIA–REPERFUSION INJURY BY INHIBITING MITOCHONDRIAL PERMEABILITY TRANSITION PORE OPENING
TLDR
The findings of the present study indicate that HSYA protects the myocardium against ischaemia–reperfusion injury by inhibiting mitochondrial permeability transition pore opening.
Controlled reperfusion after hypothermic heart preservation inhibits mitochondrial permeability transition-pore opening and enhances functional recovery.
TLDR
It is demonstrated that low-pressure reperfusion after hypothermic heart ischemia improves postischemic contractile dysfunction and attenuates necrosis and apoptosis and this protection could be related to an inhibition of mitochondrial permeability transition.
Opening of mitochondrial permeability transition pore induces hypercontracture in Ca2+ overloaded cardiac myocytes
TLDR
In permeabilized myocytes, mPTP could promote hypercontracture when cytosolic Ca2+ overload was mimicked in the presence of ATP, and was prevented when ATP was removed from the intracellular-like medium.
The Mitochondrial Permeability Transition Pore and its Role in Anaesthesia-Triggered Cellular Protection during Ischaemia-Reperfusion Injury
TLDR
It is now considered that anaesthesia-induced closure of the mPTP is the underlying effector mechanism that is responsible for the cytoprotection previously demonstrated in clinical studies investigating anaesthetic-mediated cardiac and neuroprotection.
Opening of mitochondrial permeability transition pore induces hypercontracture in Ca2+ overloaded cardiac myocytes
TLDR
mPTP opening may induce ATP-dependent hypercontracture in Ca2+ overloaded myocytes, and this phenomenon could reconcile the apparently contradictory hypotheses of hyper contracture and mPTPOpening as main determinants of necrosis during the first minutes of reperfusion.
Signalling via the reperfusion injury signalling kinase (RISK) pathway links closure of the mitochondrial permeability transition pore to cardioprotection.
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References

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TLDR
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TLDR
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TLDR
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