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Published on: July 26, 2017
Amino Acid Sensing in Skeletal Muscle
Tatiana Moro1, Scott M Ebert2, Christopher M Adams2
1Department of Nutrition and Metabolism, University of Texas Medical Branch, Galveston, TX, USA; Sealy Center on Aging, University of Texas Medical Branch, Galveston, TX, USA.
Aging impairs muscle protein synthesis, leading to weakness. Amino acid sensing pathways involving mTORC1 and ATF4 are key to muscle aging and may offer strategies to combat sarcopenia.
Area of Science:
- Gerontology
- Molecular Biology
- Skeletal Muscle Physiology
Background:
- Aging is characterized by reduced skeletal muscle protein synthesis, leading to weakness and atrophy.
- The molecular mechanisms underlying age-related muscle decline are not fully understood.
- Impaired amino acid (AA) availability is implicated in age-related muscle dysfunction.
Purpose of the Study:
- To review the role of amino acid (AA) sensing pathways in skeletal muscle aging.
- To explore the involvement of mammalian/mechanistic target of rapamycin complex 1 (mTORC1) and activating transcription factor 4 (ATF4) pathways.
- To identify potential therapeutic targets for sarcopenia.
Main Methods:
- Literature review of studies on aging, skeletal muscle protein synthesis, and AA metabolism.
- Analysis of evidence linking mTORC1 and ATF4 signaling to age-related muscle changes.
- Synthesis of findings regarding interventions targeting AA sensing pathways.
Main Results:
- Impaired AA delivery to aged skeletal muscle activates mTORC1 and ATF4 pathways.
- These pathways play a significant role in the molecular mechanisms of skeletal muscle aging.
- Interventions improving muscle mass and strength reverse age-related changes in AA delivery and signaling.
Conclusions:
- AA sensing pathways, particularly mTORC1 and ATF4, are critical in skeletal muscle aging.
- Understanding these pathways can inform strategies to prevent or treat sarcopenia.
- Targeting AA delivery and signaling pathways holds promise for mitigating age-related muscle loss.
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