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Review

Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy

1
Heart and Vascular Institute, John W. Deming Department of Medicine, Tulane University School of Medicine, 1430 Tulane Ave SL-48, New Orleans, LA 70112, USA
2
Department of Physiology, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA 70112, USA
*
Authors to whom correspondence should be addressed.
Cells 2020, 9(9), 1970; https://doi.org/10.3390/cells9091970
Received: 1 July 2020 / Revised: 18 August 2020 / Accepted: 19 August 2020 / Published: 26 August 2020
(This article belongs to the Special Issue Insulin-Like Growth Factors in Development, Cancers and Aging)
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 NF-κΒ and Smad pathways, respectively. Several miRNAs have been found to regulate IGF-1 signaling in skeletal muscle, and these miRs are likely regulated in different pathological conditions and contribute to the development of muscle atrophy. IGF-1 also potentiates skeletal muscle regeneration via activation of skeletal muscle stem (satellite) cells, which may contribute to muscle hypertrophy and/or inhibit atrophy. Importantly, IGF-1 levels and IGF-1R downstream signaling are suppressed in many chronic disease conditions and likely result in muscle atrophy via the combined effects of altered protein synthesis, UPS activity, autophagy, and muscle regeneration. View Full-Text
Keywords: insulin-like growth factor-1; skeletal muscle; hypertrophy; atrophy; cachexia; muscle regeneration; autophagy insulin-like growth factor-1; skeletal muscle; hypertrophy; atrophy; cachexia; muscle regeneration; autophagy
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MDPI and ACS Style

Yoshida, T.; Delafontaine, P. Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy. Cells 2020, 9, 1970. https://doi.org/10.3390/cells9091970

AMA Style

Yoshida T, Delafontaine P. Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy. Cells. 2020; 9(9):1970. https://doi.org/10.3390/cells9091970

Chicago/Turabian Style

Yoshida, Tadashi, and Patrice Delafontaine. 2020. "Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy" Cells 9, no. 9: 1970. https://doi.org/10.3390/cells9091970

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