mTor Signaling in Skeletal Muscle During Sepsis and Inflammation: Where Does It All Go Wrong?

Robert A. Frost, Charles H. Lang

Abstract

The mammalian target of rapamycin (mTOR) is an evolutionarily conserved protein kinase that exquisitely regulates protein metabolism in skeletal muscle. mTOR integrates input from amino acids, growth factors, and intracellular cues to make or break muscle protein. mTOR accomplishes this task by stimulating the phosphorylation of substrates that control protein translation while simultaneously inhibiting proteasomal and autophagic protein degradation. In a metabolic twist of fate, sepsis induces muscle atrophy in part by the aberrant regulation of mTOR. In this review, we track the steps of normal mTOR signaling in muscle and examine where they go astray in sepsis and inflammation.

Footnotes

  • This work was supported in part by National Institute of General Medicine Sciences Grant GM-38032.

  • No conflicts of interest, financial or otherwise, are declared by the author(s).

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