Research articleExtraocular, limb and diaphragm muscle group-specific antioxidant enzyme activity patterns in control and mdx mice
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Fulminant lymphocytic myocarditis associated with orbital myositis and diaphragmatic paralysis
2016, Cardiovascular PathologyCitation Excerpt :Lymphocytic myocarditis with skeletal muscle myositis is a rare condition, although the literature does contain previous reports [2–4]. However, the case presented here is unique; the involved skeletal muscles (diaphragm and EOM) differ, in terms of functional and structural characteristics, to the limb muscles [5,6] involved in previous reports [3,4]. The other notable finding in this case was that immunosuppressive therapy was effective in suppressing the concomitant fulminant lymphocytic myocarditis and myositis.
X-ROS signaling in the heart and skeletal muscle: Stretch-dependent local ROS regulates [Ca<sup>2+</sup>]<inf>i</inf>
2013, Journal of Molecular and Cellular CardiologyCitation Excerpt :In support of such speed in redox reversibility, if spark rate is elevated by an acute application of low dose H2O2, spark rate can be returned to normal within seconds of wash out of H2O2 [1]. Interestingly, this reversibility is compromised in mdx muscle [1], which is deficient in endogenous reducing systems [48]. A seemingly overwhelming number of cardiac enzymes, kinases, phosphatases, channels, exchangers, pumps, and transcription factors have been shown to be redox-sensitive in vitro (reviewed in Ref. [7,49]), blurring the potential downstream targets of X-ROS signaling.
Increased oxidative stress in dystrophin deficient (mdx) mice masticatory muscles
2011, Experimental and Toxicologic PathologyCitation Excerpt :The different morphological response of tongue muscle to dystrophin deficiency as compared with mdx masseter and temporal muscles could be explained with the different cellular antioxidant capacity among various muscles (Oh-Ishi, 1995; Powers, 1994). Such differences in cell protective mechanisms may explain why a disease resulting from a genetic defect could be manifested differently over space and time (Ragusa, 1996; Rando, 1998). Nevertheless, the observed increased oxidative stress in mdx masticatory musles might be a secondary effect and/or a consequence of inflammatory processes and muscle adaptations to dystrophinopathy such as degeneration and regeneration.
Pathological pattern of Mdx mice diaphragm correlates with gradual expression of the short utrophin isoform Up71
2006, Biochimica et Biophysica Acta - Molecular Basis of DiseaseBiological organization of the extraocular muscles
2006, Progress in Brain ResearchCitation Excerpt :Here, we briefly review only some of the diseases where the EOM is divergent from most other skeletal muscles. EOM is completely spared in Duchenne (Karpati and Carpenter, 1986; Kaminski et al., 1992; Khurana et al., 1995; Ragusa et al., 1996, 1997; Porter, 1998), limb girdle (Porter et al., 2001b), and congenital (Porter and Karathanasis, 1998) muscular dystrophy. By contrast, EOM is preferentially affected in oculopharyngeal muscular dystrophy, which exhibits a different pathogenic mechanism from the other muscular dystrophies (Brais et al., 1998).