Journal
CELL REPORTS
Volume 21, Issue 6, Pages 1507-1520Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.10.040
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Funding
- ERC [338999]
- BBSRC [BB/GO18049/1]
- European Commission Programme SYNERGY-COPD [270086]
- BBSRC [BB/N022548/1, BB/K003860/1] Funding Source: UKRI
- MRC [MR/M009114/1, MR/M012573/1, MR/P020941/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/K003860/1, BB/N022548/1] Funding Source: researchfish
- Medical Research Council [MR/M009114/1, MR/M012573/1, MR/P020941/1] Funding Source: researchfish
- European Research Council (ERC) [338999] Funding Source: European Research Council (ERC)
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Regular endurance training improves muscle oxidative capacity and reduces the risk of age-related disorders. Understanding the molecular networks underlying this phenomenon is crucial. Here, by exploiting the power of computational modeling, we show that endurance training induces profound changes in gene regulatory networks linking signaling and selective control of translation to energy metabolism and tissue remodeling. We discovered that knockdown of the mTOR-independent factor Eif6, which we predicted to be a key regulator of this process, affects mitochondrial respiration efficiency, ROS production, and exercise performance. Our work demonstrates the validity of a data-driven approach to understanding muscle homeostasis.
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