Differential response of skeletal muscles to mTORC1 signaling during atrophy and hypertrophy.

ABSTRACT:

Background

Skeletal muscle mass is determined by the balance between protein synthesis and degradation. Mammalian target of rapamycin complex 1 (mTORC1) is a master regulator of protein translation and has been implicated in the control of muscle mass. Inactivation of mTORC1 by skeletal muscle-specific deletion of its obligatory component raptor results in smaller muscles and a lethal dystrophy. Moreover, raptor-deficient muscles are less oxidative through changes in the expression PGC-1α, a critical determinant of mitochondrial biogenesis. These results suggest that activation of mTORC1 might be beneficial to skeletal muscle by providing resistance to muscle atrophy and increasing oxidative function. Here, we tested this hypothesis by deletion of the mTORC1 inhibitor tuberous scle

SUBMITTER: Bentzinger CF 

PROVIDER: S-EPMC3622636 | biostudies-literature | 2013 Mar

REPOSITORIES: biostudies-literature