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EnglishSkeletal muscle atrophy is a debilitating response to fasting, disuse, cancer, and other systemic diseases. In atrophying muscles, the ubiquitin ligase, atrogin-1 (MAFbx), is dramatically induced, and this response is necessary for rapid atrophy. Here, we show that in cultured myotubes undergoing atrophy, the activity of the PI3K/AKT pathway decreases, leading to activation of Foxo transcription factors and atrogin-1 induction. IGF-1 treatment or AKT overexpression inhibits Foxo and atrogin-1 expression. Moreover, constitutively active Foxo3 acts on the atrogin-1 promoter to cause atrogin-1 transcription and dramatic atrophy of myotubes and muscle fibers. When Foxo activation is blocked by a dominant-negative construct in myotubes or by RNAi in mouse muscles in vivo, atrogin-1 induction during starvation and atrophy of myotubes induced by glucocorticoids are prevented. Thus, forkhead factor(s) play a critical role in the development of muscle atrophy, and inhibition of Foxo factors is an attractive approach to combat muscle wasting.
Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy / Sandri, Marco; Sandri, Claudia; Gilbert, Alex; Skurk, Carsten; Calabria, Elisa; Picard, Anne; Walsh, Kenneth; Schiaffino, Stefano; Lecker, Stewart H; Goldberg, Alfred L. - In: CELL. - ISSN 0092-8674. - STAMPA. - 117:3(2004), pp. 399-412.
| Titolo: | Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy |
| Autori: | |
| Data di pubblicazione: | 2004 |
| Rivista: | |
| Citazione: | Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy / Sandri, Marco; Sandri, Claudia; Gilbert, Alex; Skurk, Carsten; Calabria, Elisa; Picard, Anne; Walsh, Kenneth; Schiaffino, Stefano; Lecker, Stewart H; Goldberg, Alfred L. - In: CELL. - ISSN 0092-8674. - STAMPA. - 117:3(2004), pp. 399-412. |
| Handle: | http://hdl.handle.net/11562/954317 |
| Appare nelle tipologie: | 01.01 Articolo in Rivista |
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