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  • Title: PGC-1α over-expression suppresses the skeletal muscle atrophy and myofiber-type composition during hindlimb unloading.
    Author: Wang J, Wang F, Zhang P, Liu H, He J, Zhang C, Fan M, Chen X.
    Journal: Biosci Biotechnol Biochem; 2017 Mar; 81(3):500-513. PubMed ID: 27869526.
    Abstract:
    Disuse leads to severe muscle atrophy and a slow-to-fast myofiber-type transition. PGC-1α (Peroxisome proliferator-activated receptor γ coactivator 1α) is documented to play an important role in muscle atrophy and slow-twitch myofiber determination. Transcription of atrophy-related Atrogin-1 by FoxO3 can be reduced by PGC-1α. While Smad3 augments FoxO3-induced Atrogin-1 and MuRF1 promoter activity. So PGC-1α, as a transcription co-activator, may regulate hindlimb unloading (HU)-induced myofiber-type transition and muscle atrophy through Smad3. Our results showed that transgenic PGC-1α mice resisted HU-induced muscle loss, atrophy-related genes expression, and slow-to-fast myofiber-type transition. Furthermore, over-expression of PGC-1α resisted the increase in pSmad3 during muscle atrophy in vivo and in vitro. And, PGC-1α over-expression inhibited the expression of atrogenes via suppressing the phosphorylation of Smad3 in vitro. Thus, PGC-1α is effective in regulating myofiber-type transition during HU, and it alleviates skeletal muscle atrophy partially through suppressing the activation of Smad3.
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