Long-term treatment with naproxcinod significantly improves skeletal and cardiac disease phenotype in the mdx mouse model of dystrophy.

@article{Uaesoontrachoon2014LongtermTW,
  title={Long-term treatment with naproxcinod significantly improves skeletal and cardiac disease phenotype in the mdx mouse model of dystrophy.},
  author={Kitipong Uaesoontrachoon and James L. Quinn and Kathleen S. Tatem and Jack H Van der Meulen and Qing Yu and Aditi Phadke and Brittany K Miller and Heather Gordish-Dressman and Ennio Ongini and Daniela Miglietta and Kanneboyina Nagaraju},
  journal={Human molecular genetics},
  year={2014},
  volume={23 12},
  pages={3239-49}
}
In Duchenne muscular dystrophy (DMD) patients and the mouse model of DMD, mdx, dystrophin deficiency causes a decrease and mislocalization of muscle-specific neuronal nitric oxide synthase (nNOSμ), leading to functional impairments. Previous studies have shown that nitric oxide (NO) donation associated with anti-inflammatory action has beneficial effects in dystrophic mouse models. In this study, we have systematically investigated the effects of naproxcinod, an NO-donating naproxen derivative… CONTINUE READING
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