Myocardial ischemia/reperfusion causes VDAC phosphorylation which is reduced by cardioprotection with a p38 MAP kinase inhibitor.

@article{Schwertz2007MyocardialIC,
  title={Myocardial ischemia/reperfusion causes VDAC phosphorylation which is reduced by cardioprotection with a p38 MAP kinase inhibitor.},
  author={Hansj{\"o}rg Schwertz and Justin M Carter and Mulati Abdudureheman and Martin Russ and Ute Buerke and Axel Schlitt and Ursula Mueller-Werdan and Roland Prondzinsky and Karl Werdan and Michael Buerke},
  journal={Proteomics},
  year={2007},
  volume={7 24},
  pages={4579-88}
}
Myocardial ischemia (MI) and reperfusion (R) results in activation of the p38 MAP kinase pathway. This pathway phosphorylates transcription factors and cytoplasmic proteins leading to expression of adhesion molecules and cytokines, increased neutrophil activation, and finally, myocardial necrosis and apoptosis. We studied the effects of a p38 MAP kinase inhibitor, PD169316, on cardioprotection, protein expression, and tyrosine phosphorylation, in a rabbit model of 1 h of (MI) and 3 h of (R… CONTINUE READING