ArticleFrontiers in aging neuroscience2014
New pathobiochemical insights into dystrophinopathy from the proteomics of senescent mdx mouse muscle.
Article in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 8 citations in OpenAlex.
- Multiomic Approaches to Uncover the Complexities of Dystrophin-Associated Cardiomyopathy.International journal of molecular sciences · 2021Review
- Progressive muscle proteome changes in a clinically relevant pig model of Duchenne muscular dystrophy.Scientific reports · 2016Article
- Elastase levels and activity are increased in dystrophic muscle and impair myoblast cell survival, proliferation and differentiation.Scientific reports · 2016Article
- Editorial: Pathophysiological Mechanisms of Sarcopenia in Aging and in Muscular Dystrophy: A Translational Approach.Frontiers in aging neuroscience · 2015Article
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3 authors at 1 institution in 1 country.
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Abstract
Primary abnormalities in the dystrophin gene cause X-linked muscular dystrophy, a highly progressive muscle wasting disorder of childhood. A spontaneous animal model of Duchenne muscular dystrophy is the mdx mouse, which presents a highly interesting phenotype that exhibits considerable variations in the degree of fiber degeneration in different subtypes of muscles. The idea that aging exacerbates the dystrophic mdx phenotype, as previously indicated by a large number of biochemical and cell biological studies, was clearly confirmed by comparative muscle proteomics. Here we outline recent findings of age-dependent changes in the dystrophin-deficient muscle proteome and contrast these results with the previously established proteomic profile of sarcopenic muscle. Besides comparable perturbations of various biochemical functions, especially striking are similarities in the cellular stress response associated with a drastic up-regulation of small αB-crystallin-like heat shock proteins. Hence, the comparison of large-scale proteomic data sets of natural muscle aging with dystrophic sarcopenia promises to shed light on the differential effect of sarcopenia of old age vs. senescent abnormalities on a mutant dystrophic background.
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