Preconditioning and postconditioning: the essential role of the mitochondrial permeability transition pore.

@article{Lim2007PreconditioningAP,
  title={Preconditioning and postconditioning: the essential role of the mitochondrial permeability transition pore.},
  author={Shiang Y. Lim and Sean M. Davidson and Derek J. Hausenloy and Derek M. Yellon},
  journal={Cardiovascular research},
  year={2007},
  volume={75 3},
  pages={
          530-5
        }
}
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286 Citations
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286 Citations

The mitochondrial permeability transition pore as a target for preconditioning and postconditioning
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[Role of mitochondrial permeability transition pore in mediating the effect of endomorphin-1 postconditioning against myocardial ischemia-reperfusion injury in rats].
TLDR
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The MPTP status during early reoxygenation is critical for cardioprotection.
Postconditioning inhibits mPTP opening independent of oxidative phosphorylation and membrane potential.
Morphine Postconditioning Protects Against Reperfusion Injury: the Role of Protein Kinase C-Epsilon, Extracellular Signal-Regulated Kinase 1/2 and Mitochondrial Permeability Transition Pores
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It is suggested that MpostC protects isolated rat hearts against ischemia-reperfusion injury via activating PKCε-ERK1/2 pathway and inhibiting mPTP opening and Cyt-c release.
Participation of mitochondrial permeability transition pore in the effects of ischemic preconditioning in hypertrophied hearts: role of NO and mitoKATP.
Mitochondrial cyclophilin-D as a critical mediator of ischaemic preconditioning
TLDR
The cyclophilin-D component of the mPTP is required by IPC to generate mitochondrial ROS and phosphorylate Akt and Erk1/2, major steps in the IPC signalling pathway.
Mechanisms involved in postconditioning protection of cardiomyocytes against acute reperfusion injury.
Morphine Postconditioning Protects against Reperfusion Injury via Inhibiting JNK/p38 MAPK and Mitochondrial Permeability Transition Pores Signaling Pathways
TLDR
It is suggested that MpostC protects isolated rat hearts against reperfusion injury via inhibiting JNK/p38 MAPKs and mitochondrial permeability transition pores signaling pathways.
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References

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Preconditioning protects by inhibiting the mitochondrial permeability transition.
TLDR
In conclusion, preconditioning protects the myocardium by reducing the probability of the mPT, which normally occurs during ischemia-reperfusion in response to oxidative stress.
Inhibiting mitochondrial permeability transition pore opening at reperfusion protects against ischaemia-reperfusion injury.
Transient Mitochondrial Permeability Transition Pore Opening Mediates Preconditioning-Induced Protection
TLDR
It is hypothesized that transient mPTP opening and ROS mediate the protection associated with myocardial preconditioning and mitochondrial uncoupling.
PI 3-kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning.
Postconditioning Inhibits Mitochondrial Permeability Transition
TLDR
Postconditioning inhibits opening of the mPTP and provides a powerful antiischemic protection.
Ischaemic Preconditioning Inhibits Opening of Mitochondrial Permeability Transition Pores in the Reperfused Rat Heart
TLDR
It is demonstrated that IPC inhibits initial MPTP opening in hearts reperfused after 30 min global ischaemia, and subsequently enhances pore closure as hearts recover, suggesting that protection from reperfusion injury is better achieved by reducing factors that induce MPTPOpening than by inhibiting the MPTP directly.
Signalling via the reperfusion injury signalling kinase (RISK) pathway links closure of the mitochondrial permeability transition pore to cardioprotection.
Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death
TLDR
Cyclophilin D and the mitochondrial permeability transition are required for mediating Ca2+- and oxidative damage-induced cell death, but not Bcl-2 family member-regulated death.
Properties of the Permeability Transition Pore in Mitochondria Devoid of Cyclophilin D*
TLDR
The experiments demonstrate that the PTP can form and open, that CyP-D represents the target for PTP inhibition by CsA, and that Cyp-D modulates the sensitivity of the P TP to Ca2+ but not its regulation by the proton electrochemical gradient, adenine nucleotides, and oxidative stress.
Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion.
TLDR
Using isolated heart mitochondria, it was demonstrated that pore opening could become CsA-insensitive under conditions of adenine nucleotide depletion and high matrix [Ca2+] such as may occur during the initial phase of reperfusion.
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