Cardiac-specific overexpression of E40K active Akt prevents pressure overload-induced heart failure in mice by increasing angiogenesis and reducing apoptosis

@article{Ceci2007CardiacspecificOO,
  title={Cardiac-specific overexpression of E40K active Akt prevents pressure overload-induced heart failure in mice by increasing angiogenesis and reducing apoptosis},
  author={Marcello Ceci and Paolo Gallo and Marco Santonastasi and Serena Grimaldi and Michael V. G. Latronico and Angela Pitisci and Ewa Missol-Kolka and Maria Cecilia Scimia and Daniele Catalucci and Denise Hilfiker-Kleiner and Gianluigi Condorelli},
  journal={Cell Death and Differentiation},
  year={2007},
  volume={14},
  pages={1060-1062}
}
Physiological myocardial hypertrophy is the result of adaptation of the heart to increased work demands on the cardiovascular system. This response is mediated by pathways which trigger increased protein synthesis and the consequent growth in cardiomyocyte (CMC) size. Multiple signaling pathways contribute to the physiological hypertrophy phenotype, of which one well studied is the IGF1-PI3K-Akt pathway. This pathway is also involved in the mechanism of action of pro-angiogenic factors like… CONTINUE READING