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
        }
}

Figures and Tables from this paper

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TLDR
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TLDR
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The Mitochondrial Permeability Transition Pore and its Role in Anaesthesia-Triggered Cellular Protection during Ischaemia-Reperfusion Injury
TLDR
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Opening of mitochondrial permeability transition pore induces hypercontracture in Ca2+ overloaded cardiac myocytes
TLDR
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Inhibiting mitochondrial permeability transition pore opening: a new paradigm for myocardial preconditioning?
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TLDR
It is shown that in isolated perfused rat hearts subjected to 30 min ischemia and 15 min reperfusion, 0.2 microM cyclosporin A restored the ATP/ADP ratio and AMP content to pre-ischemic values.
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TLDR
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TLDR
Preventing the rise of pHi after reperfusion blocked the MPT, improved ATP recovery, and prevented cell death was associated with recovery of 30-40% of ATP.
Opening of the Mitochondrial Permeability Transition Pore Causes Depletion of Mitochondrial and Cytosolic NAD+and Is a Causative Event in the Death of Myocytes in Postischemic Reperfusion of the Heart*
TLDR
Upon reperfusion after prolonged ischemia, PTP opening in the heart can be documented as a CsA-sensitive release of NAD+, which is then partly degraded by glycohydrolase and partly released when sarcolemmal integrity is compromised.
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TLDR
It is concluded that simulated reperfusion significantly augments the cellular membrane damage elicited by simulated ischemia in isolated cardiomyocytes devoid of other factors and suggested that reactive oxygen species, perhaps from the mitochondria, participate in this injury.
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TLDR
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TLDR
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TLDR
Increased mitochondrial ROS generation initiates a destructive cycle involving Ca2+ release from stores and mitochondrial Ca2-loading, which further increases ROS production and culminates in opening of the mPTP and necrotic cell death in primary brain cells.
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