Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy
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Abstract
Insulin-like growth factor-1 (IGF-1) is a key growth factor that regulates both anabolic and catabolic pathways in skeletal muscle. IGF-1 increases skeletal muscle protein synthesis via PI3K/Akt/mTOR and PI3K/Akt/GSK3β pathways. PI3K/Akt can also inhibit FoxOs and suppress transcription of E3 ubiquitin ligases that regulate ubiquitin proteasome system (UPS)-mediated protein degradation. Autophagy is likely inhibited by IGF-1 via mTOR and FoxO signaling, although the contribution of autophagy regulation in IGF-1-mediated inhibition of skeletal muscle atrophy remains to be determined. Evidence has suggested that IGF-1/Akt can inhibit muscle atrophy-inducing cytokine and myostatin signaling via inhibition of the…
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Authors
2Topics & keywords
Topics
Keywords
- Skeletal muscle
- PI3K/AKT/mTOR pathway
- Protein kinase B
- Muscle atrophy
- Autophagy
- Myostatin
- Muscle hypertrophy
- Biology
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Funding
- AHAmerican Heart AssociationAwards: 19TPA34850165, 15SDG25240022
- NINational Institutes of HealthAwards: 20GM103629, R01HL080682, U54GM104940, P30GM103337, R01HL070241
- NHNational Heart, Lung, and Blood InstituteAwards: R01HL080682, R01HL070241
- NINational Institute of General Medical SciencesAwards: P30GM103337, U54GM104940