Overexpression of calpastatin by gene transfer prevents troponin I degradation and ameliorates contractile dysfunction in rat hearts subjected to ischemia/reperfusion.

@article{Maekawa2003OverexpressionOC,
  title={Overexpression of calpastatin by gene transfer prevents troponin I degradation and ameliorates contractile dysfunction in rat hearts subjected to ischemia/reperfusion.},
  author={Atsuo Maekawa and Jong-Kook Lee and Takashi Nagaya and Kaichiro Kamiya and Kenji Yasui and Mitsuru Horiba and Keiko Miwa and Mahmud Uzzaman and Masatoshi Maki and Yuichi Ueda and Itsuo Kodama},
  journal={Journal of molecular and cellular cardiology},
  year={2003},
  volume={35 10},
  pages={1277-84}
}
Calpain is a Ca(2+)-activated neutral protease that supposedly plays a key role in myocardial dysfunction following ischemia/reperfusion, by degrading certain proteins involved in the contraction mechanism. It is possible that overexpression of calpastatin, an endogenous calpain inhibitor, lessens contractile dysfunction in the heart after reperfusion by preventing cardiac troponin I (TnI) degradation. This claim is tested by overexpression of human calpastatin (hCS) in rat hearts ex vivo using… CONTINUE READING