期刊
NATURE CELL BIOLOGY
卷 3, 期 11, 页码 1009-1013出版社
MACMILLAN PUBLISHERS LTD
DOI: 10.1038/ncb1101-1009
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Skeletal muscle is composed of multinucleated fibres, formed after the differentiation and fusion of myoblast precursors'. Skeletal muscle atrophy and hypertrophy refer to changes in the diameter of these pre-existing muscle fibres. The prevention of atrophy would provide an obvious clinical benefit; insulin-like growth factor 1 (IGF-1) is a promising anti-atrophy agent(2-5) because of its ability to promote hypertrophy. However, the signalling pathways by which IGF-1 promotes hypertrophy remain unclear, with roles suggested for both the calcineurin/NFAT (nuclear factor of activated T cells) pathway(6,7) and the Ptdlns-3-OH kinase (PI(3)K)/Akt pathway(8). Here we employ a battery of approaches to examine these pathways during the hypertrophic response of cultured myotubes to IGF-1, We report that Akt promotes hypertrophy by activating downstream signalling pathways previously implicated in activating protein synthesis: the pathways downstream of mammalian target of rapamycin (mTOR) and the, pathway activated by phosphorylating and thereby inhibiting glycogen synthase kinase 3 (GSK3). In contrast, in addition to demonstrating that calcineurin does not mediate IGF-1-induced hypertrophy, we show that IGF-1 unexpectedly acts via Akt to antagonize calcineurin signalling during myotube hypertrophy.
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