Cited by 80Muscle Physiology and DisordersNutrition and Health in AgingSpaceflight effects on biology

Skeletal Muscle Atrophy: Discovery of Mechanisms and Potential Therapies

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Ebert, Scott M., Al-Zougbi, Asma, Bodine, Sue C., Adams, Christopher M.·2019·Physiology

Abstract

Skeletal muscle atrophy proceeds through a complex molecular signaling network that is just beginning to be understood. Here, we discuss examples of recently identified molecular mechanisms of muscle atrophy and how they highlight an immense need and opportunity for focused biochemical investigations and further unbiased discovery work.

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Crossref · 10.1152/physiol.00003.2019

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54 of 54 references verified0 citation errors · 0 not checkable

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  • Activation of IGF-1/PI3K/Akt signaling represses MAFbx and MuRF1 gene expression via decreasing FoxO expression and activity.

    “On the contrary, the activation of insulin-like growth factor (IGF-1)/phosphoinositide 3-kinase (PI3K)/Akt signaling pathway represses the MAFbx and MuRF1 gene expression via decreasing the expression and activity of FoxO.”
  • Activation of IGF-1/PI3K/Akt pathway stimulates protein synthesis and induces muscle growth via mTOR kinase.

    “In addition to inhibiting muscle atrophy, the activation of insulin-like growth factor 1 (IGF-1)/PI3K/Akt pathway also stimulates protein synthesis and induces muscle growth via rapamycin complex (mTOR) kinase [5].”
  • Under starvation, muscle disuse, glucocorticoid excess, and aging, glucocorticoid receptor and FoxO increase MuRF1 expression and promote muscle atrophy.

    “Under a wide range of conditions including starvation, muscle disuse, glucocorticoid excess, and aging, the glucocorticoid receptor and transcription factor forkhead box O (FoxO) increase the expression of MuRF1 and promote muscle atrophy [5].”

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Authors
Ebert, S. M., Al-Zougbi, A., Bodine, S. C., & Adams, C. M.
Affiliations
  • University of Iowa (US)
  • Departments of Internal Medicine and Molecular Physiology and Biophysics, and the Fraternal Order of Eagles Diabetes Research Center, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, Iowa
Corresponding author
Adams, Christopher M.
Venue
Physiology
Published
2019-07-01
Volume
34
Issue
4
Pages
232-239
ISSN
  • 0886-1714 (ISSN-L)
  • 1548-9213
  • 1548-9221
OpenAlex
W2948588968
Cited by
80
References
53
Citations by year
2026: 3 · 2025: 9 · 2024: 8 · 2023: 13 · 2022: 15 · 2021: 15 · 2020: 12 · 2019: 4 · 2013: 1
FWCI
1.02
Type
journal article
Language
en
Open access
Locations
  • Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • NIH (R01AR071762, R01AG060637, R44AG047684)
  • US Department of Veterans Affairs (I01BX00976)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
  • Health Sciences › Medicine › Physiology › Spaceflight effects on biology
Keywords
skeletal muscle atrophy, molecular signaling networks, therapeutic target, muscle protein degradation
MeSH terms
Animals, Humans, Muscular Atrophy, Signal Transduction, Muscle, Skeletal

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