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It has been suggested that the first step in blocking mitochondria trafficking along the axon is carried out by the Ca 2+ -dependent release of mitochondria from microtubules involving the combined actions of the key adaptors of kinesins and dyneins, Miro/Milton, and syntaphilin (SNPH) [46, 47]

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These results are consistent with the major features of hind-limb suspension-related phenotypes of skeletal muscles as an index of anti-gravity muscle atrophy 66 , thus assuring that the experimental design including the mouse age and muscle-disuse period (in vivo assay time-point) were appropriate to the conclusion that 3-days LASSS oral-administration prevents tyrosine-residue nitration of extracellular HGF (Y198) during 5-days muscle disuse

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