A novel computational model of mouse myocyte electrophysiology to assess the synergy between Na+ loading and CaMKII.

@article{Morotti2014ANC,
  title={A novel computational model of mouse myocyte electrophysiology to assess the synergy between Na+ loading and CaMKII.},
  author={Stefano Morotti and Andrew G. Edwards and Andrew D. McCulloch and Donald M. Bers and Eleonora Grandi},
  journal={The Journal of physiology},
  year={2014},
  volume={592 6},
  pages={1181-97}
}
Ca(2+)-calmodulin-dependent protein kinase II (CaMKII) hyperactivity in heart failure causes intracellular Na(+) ([Na(+)]i) loading (at least in part by enhancing the late Na(+) current). This [Na(+)]i gain promotes intracellular Ca(2+) ([Ca(2+)]i) overload by altering the equilibrium of the Na(+)-Ca(2+) exchanger to impair forward-mode (Ca(2+) extrusion), and favour reverse-mode (Ca(2+) influx) exchange. In turn, this Ca(2+) overload would be expected to further activate CaMKII and thereby… CONTINUE READING
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