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Vitiello L, Marabita M, Sorato E, et al. Drug Repurposing for Duchenne Muscular Dystrophy: The Monoamine Oxidase B Inhibitor Safinamide Ameliorates the Pathological Phenotype in . Front Physiol. 2018;9:1087doi: 10.3389/fphys.2018.01087.
Vitiello, L., Marabita, M., Sorato, E., Nogara, L., Forestan, G., Mouly, V., Salviati, L., Acosta, M., Blaauw, B., & Canton, M. (2018). Drug Repurposing for Duchenne Muscular Dystrophy: The Monoamine Oxidase B Inhibitor Safinamide Ameliorates the Pathological Phenotype in . Frontiers in physiology, 91087. https://doi.org/10.3389/fphys.2018.01087
Vitiello, Libero, et al. "Drug Repurposing for Duchenne Muscular Dystrophy: The Monoamine Oxidase B Inhibitor Safinamide Ameliorates the Pathological Phenotype in ." Frontiers in physiology vol. 9 (2018): 1087. doi: https://doi.org/10.3389/fphys.2018.01087
Vitiello L, Marabita M, Sorato E, Nogara L, Forestan G, Mouly V, Salviati L, Acosta M, Blaauw B, Canton M. Drug Repurposing for Duchenne Muscular Dystrophy: The Monoamine Oxidase B Inhibitor Safinamide Ameliorates the Pathological Phenotype in . Front Physiol. 2018 Aug 14;9:1087. doi: 10.3389/fphys.2018.01087. eCollection 2018. PMID: 30154729; PMCID: PMC6102489.
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Front Physiol. 2018 Aug 14;9:1087. doi: 10.3389/fphys.2018.01087. eCollection 2018.

Drug Repurposing for Duchenne Muscular Dystrophy: The Monoamine Oxidase B Inhibitor Safinamide Ameliorates the Pathological Phenotype in .

Frontiers in physiology

Libero Vitiello, Manuela Marabita, Elisa Sorato, Leonardo Nogara, Giada Forestan, Vincent Mouly, Leonardo Salviati, Manuel Acosta, Bert Blaauw, Marcella Canton

Affiliations

  1. Department of Biology, University of Padova, Padova, Italy.
  2. Interuniversity Institute of Myology, Padova, Italy.
  3. Venetian Institute of Molecular Medicine (VIMM), Padova, Italy.
  4. Department of Biomedical Sciences, University of Padova, Padova, Italy.
  5. UMRS 974 UPMC-INSERM, Center for Research in Myology, Paris, France.
  6. Fondazione Istituto di Ricerca Pediatrica Città della Speranza - IRP, Padova, Italy.

PMID: 30154729 PMCID: PMC6102489 DOI: 10.3389/fphys.2018.01087

Abstract

Oxidative stress and mitochondrial dysfunction play a crucial role in the pathophysiology of muscular dystrophies. We previously reported that the mitochondrial enzyme monoamine oxidase (MAO) is a relevant source of reactive oxygen species (ROS) not only in murine models of muscular dystrophy, in which it directly contributes to contractile impairment, but also in muscle cells from collagen VI-deficient patients. Here, we now assessed the efficacy of a novel MAO-B inhibitor, safinamide, using

Keywords: DMD; mdx; mitochondrial ROS; monoamine oxidase; muscular dystrophy; oxidative stress; safinamide

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