Imatinib mesylate ameliorates the dystrophic phenotype in exercised mdx mice

J Neuroimmunol. 2009 Jul 25;212(1-2):93-101. doi: 10.1016/j.jneuroim.2009.05.006. Epub 2009 Jun 9.


Myofiber degeneration, inflammation, and fibrosis are remarkable features of Duchenne muscular dystrophy. We hypothesized that the administration of imatinib mesylate, an inhibitor of tyrosine kinase and TGF-beta pro-fibrogenic activity, could improve the muscular conditions in mdx mice. Four-week old mdx mice were treated and exercised for 6 weeks. Gastrocnemius and diaphragm histopathology, strength, creatine kinase, and cytokine levels were evaluated. The treated group presented increased muscular strength and decreased CK levels, injured myofibers, and inflammatory infiltrates. Pro-inflammatory cytokines and TGF-beta were also reduced, while IL-10 was increased, suggesting an immunomodulatory effect of imatinib, which can ameliorate the dystrophic phenotype in mdx mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Benzamides
  • Creatine Kinase / blood
  • Cytokines / biosynthesis
  • Cytokines / genetics
  • Imatinib Mesylate
  • Male
  • Mice
  • Muscles / pathology
  • Muscular Dystrophy, Animal / drug therapy*
  • Muscular Dystrophy, Animal / immunology
  • Muscular Dystrophy, Animal / pathology
  • Muscular Dystrophy, Duchenne / drug therapy*
  • Physical Conditioning, Animal
  • Piperazines / adverse effects
  • Piperazines / therapeutic use*
  • Protein Kinase Inhibitors / therapeutic use*
  • Pyrimidines / adverse effects
  • Pyrimidines / therapeutic use*


  • Benzamides
  • Cytokines
  • Piperazines
  • Protein Kinase Inhibitors
  • Pyrimidines
  • Imatinib Mesylate
  • Creatine Kinase