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MSTN carries out its actions via down-stream signaling of the transcription factors SMAD2 and SMAD3, which in turn negatively regulate hypertrophy independent of the cat-abolic enzyme muscle ring finger protein-1 (MuRF-1). Early research indicated that atrophic actions of MSTN were attributed to an inhibition of satellite cell activation, thus impairing protein synthetic capacity (473). Moreover, in vitro research showed that MSTN blunted satellite cell proliferation and
Science and Development of Muscle Hypertrophy26satellite cells (11). To date, HGF is the only myokine shown to stimulate dormant satellite cells to enter the cell cycle early both in vitro and in vivo(748).The active form of HGF is present in the extracellular compartment of uninjured skeletal muscle (746), and it is activated by mechanical signaling via the dystrophin-as-sociated protein complex (11). Muscular contractions alter this complex, leading to nitric oxide synthase activation, which stim-