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The cytosol accumulation of p62/SQSTM1 is a marker of the functional defect in autophagy-lysosome signaling. Indeed, the marked accumulation of p62/SQSTM1 occurs in the atrophic muscle of mdx mice [32], sarcopenic muscle of mice [33], and sporadic inclusion-body myositis of muscle fibers [34]. The present study demonstrated the marked accumulation of p62/SQSTM1 in the cytosol of muscle fibers in the denervated muscle [Fig. 4]. Thus, denervated muscle exhibits a defect of autophagy-dependent signaling. Intriguingly, resveratrol supplementation in our study significantly decreased the percentage of p62/SQSTM1-positive muscle fibers after denervation. Western blot analysis using whole muscle homogenate also indicated a small but non-significant decrease in the amount of p62/SQSTM1 proteins after denervation than those of the control diet [Fig. 5]. These results suggest that resveratrol supplementation ameliorates the autophagic defect in denervated muscle. Resveratrol is known to activate AMPK, an upstream mediator of autophagy-lysosome signaling [10, 12]. AMPK activates autophagic signaling probably by inactivating mTORC1, which inhibits this autophagic system [35, 36]. In addition, AMPK directly activates ULK1 and Beclin1 [37, 38], which are necessary molecules for the initial step of the autophagic system. Thus, resveratrol alleviates the autophagic defect by activating AMPK. Since the autophagy-lysosome system is a degradation system, the improvement in the defect of the autophagic system may induce further muscle atrophy. However, the accumulation of unnecessary degraded protein also leads to the deterioration of muscle protein synthesis and promotes further degradation. Our results suggest that the alleviation of the autophagic defect in the denervated muscle may block muscle atrophy by degrading unnecessary accumulated proteins, and recovering the protein balance.. particularly with short local preparation times, upgrade permissions. work (revisit) in molecular biology as conveyed in Chart 3 “Protein type

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