| Literature DB >> 27444066 |
Tatiana Moro1, Scott M Ebert2, Christopher M Adams2, Blake B Rasmussen3.
Abstract
Aging impairs skeletal muscle protein synthesis, leading to muscle weakness and atrophy. However, the underlying molecular mechanisms remain poorly understood. Here, we review evidence that mammalian/mechanistic target of rapamycin complex 1 (mTORC1)-mediated and activating transcription factor 4 (ATF4)-mediated amino acid (AA) sensing pathways, triggered by impaired AA delivery to aged skeletal muscle, may play important roles in skeletal muscle aging. Interventions that alleviate age-related impairments in muscle protein synthesis, strength, and/or muscle mass appear to do so by reversing age-related changes in skeletal muscle AA delivery, mTORC1 activity, and/or ATF4 activity. An improved understanding of the mechanisms and roles of AA sensing pathways in skeletal muscle may lead to evidence-based strategies to attenuate sarcopenia.Entities:
Keywords: activating transcription factor 4; general control nonderepressible 2; leucine; mammalian/mechanistic target of rapamycin complex 1; tomatidine; ursolic acid
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Year: 2016 PMID: 27444066 PMCID: PMC5075248 DOI: 10.1016/j.tem.2016.06.010
Source DB: PubMed Journal: Trends Endocrinol Metab ISSN: 1043-2760 Impact factor: 12.015