Insufficient activation of Akt upon reperfusion because of its novel modification by reduced PP2A-B55α contributes to enlargement of infarct size by chronic kidney disease

@article{Tobisawa2017InsufficientAO,
  title={Insufficient activation of Akt upon reperfusion because of its novel modification by reduced PP2A-B55α contributes to enlargement of infarct size by chronic kidney disease},
  author={Toshiyuki Tobisawa and Toshiyuki Yano and Masaya Tanno and Takayuki Miki and Atsushi Kuno and Yukishige Kimura and Satoko Ishikawa and Hidemichi Kouzu and Keitaro Nishizawa and Hideaki Yoshida and Tetsuji Miura},
  journal={Basic Research in Cardiology},
  year={2017},
  volume={112},
  pages={1-12}
}
Chronic kidney disease (CKD) increases myocardial infarct size by an unknown mechanism. Here we examined the hypothesis that impairment of protective PI3K-PDK1-Akt and/or mTORC-Akt signaling upon reperfusion contributes to CKD-induced enlargement of infarct size. CKD was induced in rats by 5/6 nephrectomy (SNx group) 4 weeks before myocardial infarction experiments, and sham-operated rats served as controls (Sham group). Infarct size as a percentage of area at risk after ischemia/reperfusion… CONTINUE READING
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