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showed evidence that Cu/Zn-superoxide dismutase (SOD, Sod1 −/− )-deficient mice showed muscle atrophy, weakness, and neuromuscular junction (NMJ) degeneration in early adulthood, similar to normal muscle aging, and the transgenic expression of SOD1 specifically prevented muscle mitochondrial function and calcium treatment defects in neurons of SOD1-deficient mice [53]
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