Chronic AMPK activation evokes the slow, oxidative myogenic program and triggers beneficial adaptations in mdx mouse skeletal muscle.

@article{Ljubicic2011ChronicAA,
  title={Chronic AMPK activation evokes the slow, oxidative myogenic program and triggers beneficial adaptations in mdx mouse skeletal muscle.},
  author={Vladimir Ljubicic and Pedro Miura and Matthew Thomas Burt and Louise Boudreault and Shiemaa Khogali and John A. Lunde and J C Renaud and Bernard J. Jasmin},
  journal={Human molecular genetics},
  year={2011},
  volume={20 17},
  pages={3478-93}
}
A therapeutic approach for Duchenne muscular dystrophy (DMD) is to up-regulate utrophin in skeletal muscle in an effort to compensate for the lack of dystrophin. We previously hypothesized that promotion of the slow, oxidative myogenic program, which triggers utrophin up-regulation, can attenuate the dystrophic pathology in mdx animals. Since treatment of healthy mice with the AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR) enhances… CONTINUE READING