Exogenous zinc protects cardiac cells from reperfusion injury by targeting mitochondrial permeability transition pore through inactivation of glycogen synthase kinase-3beta.

@article{Chanoit2008ExogenousZP,
  title={Exogenous zinc protects cardiac cells from reperfusion injury by targeting mitochondrial permeability transition pore through inactivation of glycogen synthase kinase-3beta.},
  author={Guillaume Chanoit and Sungryul Lee and Jinkun Xi and Min Zhu and Rachel A McIntosh and Robert A. Mueller and Edward A. Norfleet and Zhelong Xu},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2008},
  volume={295 3},
  pages={H1227-H1233}
}
The purpose of this study was to determine whether exogenous zinc prevents cardiac reperfusion injury by targeting the mitochondrial permeability transition pore (mPTP) via glycogen synthase kinase-3beta (GSK-3beta). The treatment of cardiac H9c2 cells with ZnCl2 (10 microM) in the presence of zinc ionophore pyrithione for 20 min significantly enhanced GSK-3beta phosphorylation at Ser9, indicating that exogenous zinc can inactivate GSK-3beta in H9c2 cells. The effect of zinc on GSK-3beta… CONTINUE READING

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