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The NMN transport is likely not indispensable to ensure sufficient cellular NAD+ levels in many tissues as the Slc12a8 deficient mouse model shows the flexibility in ensuring sufficient cellular NAD+ supply in multiple tissues

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However, conflicting evidence was presented by Goodman et al., showing that Smad3 gene transfer to skeletal muscle decreased miR-29 promoter activity, whereas Akt/mTOR activity was decreased and skeletal muscle atrophy was induced [139]