The role of the IGF-1/phosphatidylinositol 3-kinase (PI3K)/Akt pathway and atrogin-1 and MuRF-1 in SI-induced atrophy and in the amelioration of atrophy by high-load isometric contractions

Schematic representation of the role of the IGF-1/phosphatidylinositol 3-kinase (PI3K)/Akt pathway and atrogin-1 and MuRF-1 in SI-induced atrophy and in the amelioration of atrophy by high-load isometric contractions. SI was associated with a decreased level of total IRS-1, and increased phosphorylation (p) state for IRS-1 at Ser307, leading to a generalized resistance to IGF-I signals. SI had no effect on p level or p state of mTOR signaling (p70S6k and 4EBP). The p state of Akt, however, was decreased, which may be suggestive of inactivation of its signaling pathway. Akt inactivation leads to activation of Foxo action on gene transcription of catabolic markers, i.e., atrogin-1 and MuRF-1 (dashed line). SI was associated with increased mRNA levels of atrogin-1 and MuRF-1, possibly via activation of the Foxo system. Electromechanical stimulation (Stim action) appears to be effective in opposing all SI induced alterations. Boldface arrows, activation; boldface blunt bars, inhibition.

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Gene expression during inactivity-induced muscle atrophy: effects of brief bouts of a forceful contraction countermeasure. (2008) Soo J. Kim, et al. J Appl Physiol (1985). 2008 Oct;105(4):1246-1254. Figure: F9. All organisms Homo sapiens Rattus norvegicus Drosophila melanogaster

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