Journal
TRENDS IN ENDOCRINOLOGY AND METABOLISM
Volume 27, Issue 11, Pages 796-806Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2016.06.010
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Funding
- National Institutes of Health [R56 AG051267, P30 AG024832, R43 AG044898, R43 AR069400, R41 AG047684]
- Department of Veterans Affairs Biomedical Laboratory Research & Development Service [IBX000976A]
- Department of Veterans Affairs Rehabilitation Research and Development Service [1I01RX001477]
- Fraternal Order of Eagles Diabetes Research Center at the University of Iowa
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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.
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