Skeletal Muscle Atrophy: Discovery of Mechanisms and Potential Therapies
Open accessAbstract
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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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.”
From Nutraceuticals in the Prevention and Treatment of the Muscle Atrophy (2021) · cites this paper as [5]
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].”
From Nutraceuticals in the Prevention and Treatment of the Muscle Atrophy (2021) · cites this paper as [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].”
From Nutraceuticals in the Prevention and Treatment of the Muscle Atrophy (2021) · cites this paper as [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
- Publisher
- American Physiological Society
- Published
- 2019-07-01
- Volume
- 34
- Issue
- 4
- Pages
- 232-239
- ISSN
- 0886-1714 (ISSN-L)
- 1548-9213
- 1548-9221
- PMC
- PMC6863373
- 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
- green
- www.ncbi.nlm.nih.gov
- 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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