Research articleConnective tissue proliferation and growth factors in animal models of Duchenne muscular dystrophy
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Treatment and Management of Muscular Dystrophies
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2010, Neuromuscular Disorders: Treatment and ManagementUpregulation of the creatine synthetic pathway in skeletal muscles of mature mdx mice
2007, Neuromuscular DisordersCitation Excerpt :Since the mdx mouse is not severely crippled [12], has less fibrosis and more central nuclei than human DMD [10,17,18], we postulated that there may be additional compensatory molecular pathways or modifier genes in the mdx mouse that warrant further investigation. Disease-modifying factors implicated in the mdx mouse have been described [19], such as extra-cellular matrix alterations [20–23], naturally occurring and experimental up-regulation of utrophin [24–27], myostatin inhibition [28,29], calcium protein-handling protein(s) [30–32] and enhanced satellite cell function and regeneration [33–37]. While some of these modifiers are likely important in making the mdx phenotype relatively benign, many of these samemdx changes are occurring in parallel with DMD [2,12,38,39] and cannot fully account for the clear discordant phenotypic severity.
Expression profiling of cytokines and related genes in regenerating skeletal muscle after cardiotoxin injection: A role for osteopontin
2003, American Journal of PathologyCitation Excerpt :Most of them are also recognized to be increased at 96 hours after muscle injury and are related to maturation of regenerating myofibers or tissue remodeling. Throughout the period examined, the gene expressions of epidermal growth factor, transforming growth factor-β1, and FGF-2, which correlate with fibrotic changes of diseased muscle,32–34 were not highly up-regulated. Our array experiments showed that the OPN gene was one of the most prominently up-regulated genes (Tables 1 and 4).