Author: ["G C Minetti","C Colussi","R Adami","C Serra","C Mozzetta","V Parente","S Fortuni","S Straino","M Sampaolesi","M Di Padova","B Illi","P Gallinari","C Steinkühler","M C Capogrossi","V Sartorelli","R Bottinelli","C Gaetano","P L Puri"]
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Abstract
Pharmacological interventions that increase myofiber size counter the functional decline of dystrophic muscles1,2. We show that deacetylase inhibitors increase the size of myofibers in dystrophin-deficient (MDX) and α-sarcoglycan (α-SG)–deficient mice by inducing the expression of the myostatin antagonist follistatin3 in satellite cells. Deacetylase inhibitor treatment conferred on dystrophic muscles resistance to contraction-coupled degeneration and alleviated both morphological and functional consequences of the primary genetic defect. These results provide a rationale for using deacetylase inhibitors in the pharmacological therapy of muscular dystrophies.
Cite this article
Minetti, G., Colussi, C., Adami, R. et al. Functional and morphological recovery of dystrophic muscles in mice treated with deacetylase inhibitors. Nat Med 12, 1147–1150 (2006). https://doi.org/10.1038/nm1479