Exercise suppresses DEAF1 to normalize mTORC1 activity and reverse muscle aging.

Sze Mun Choy, Kah Yong Goh, Wen Xing Lee, Weiyi Jiang, Qian Gou, Priya D Gopal Krishnan, Shi Chee Ong, Kenon Chua, Nathan Harmston, Hong-Wen Tang

Program in Cancer and Stem Cell Biology, Duke-NUS Medical School, Singapore 169857, Singapore. · pubmed

Paper

Abstract

Skeletal muscle is essential for movement, respiration, and metabolism, with mTORC1 acting as a key regulator of protein synthesis and degradation. In aging muscle, mTORC1 becomes overactivated, contributing to sarcopenia, though the mechanisms remain unclear. Here, we identify DEAF1, a FOXO-regulated transcription factor, as a key upstream driver of mTORC1 in aged muscle. Elevated

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Research summary

Exercise reduces DEAF1 levels to normalize mTORC1 activity and reverse muscle aging. This study addresses the mechanisms of muscle aging and suggests a potential intervention to mitigate sarcopenia, which is directly related to the aging process.

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