Implications of Insulin-Like Growth Factor-1 in Skeletal Muscle and Various Diseases
Open accessAbstract
Skeletal muscle is an essential tissue that attaches to bones and facilitates body movements. Insulin-like growth factor-1 (IGF-1) is a hormone found in blood that plays an important role in skeletal myogenesis and is importantly associated with muscle mass entity, strength development, and degeneration and increases the proliferative capacity of muscle satellite cells (MSCs). IGF-1R is an IGF-1 receptor with a transmembrane location that activates PI3K/Akt signaling and possesses tyrosine kinase activity, and its expression is significant in terms of myoblast proliferation and normal muscle mass maintenance. IGF-1 synthesis is elevated in MSCs of injured muscles and stimulates MSCs proliferation and myogenic differentiation. Mechanical loading also affects skeletal muscle production by IGF-1, and low IGF-1 levels are associated with low handgrip strength and poor physical performance. IGF-1 is potentially useful in the management of Duchenne muscular dystrophy, muscle atrophy, and promotes neurite development. This review highlights the role of IGF-1 in skeletal muscle, its importance during myogenesis, and its involvement in different disease conditions.
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IGF-1 levels are inhibited in numerous chronic diseases, including sarcopenia, potentially leading to muscle atrophy resulting from altered protein synthesis, ubiquitin-proteasome system activity, autophagy, and impaired muscle regeneration.
“However, IGF-1 levels are inhibited in numerous chronic diseases, including sarcopenia, potentially leading to muscle atrophy resulting from the combined impacts of altered protein synthesis, ubiquitin-proteasome system (UPS) activity, autophagy, and impaired muscle regeneration [107].”
From Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis (2025) · cites this paper as [107]
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Fibromodulin modulates myoblast differentiation by controlling calcium channel
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Self-citationMyostatin regulates pituitary development and hepatic IGF1
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Self-citationTherapeutic Study of Phytochemicals Against Cancer and Alzheimer’s Disease Management
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Off-Label Use of Recombinant IGF-I to Promote Growth: Is It Appropriate?
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Self-citation
Flagged first, then by citations
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- Authors
- Ahmad, S. S., Ahmad, K., Lee, E. J., Lee, Y.-H., & Choi, I.
- Affiliations
- Yeungnam University (KR)
- Daegu Catholic University (KR)
- Corresponding author
- Lee, Yong-Ho
- Choi, Inho
- Venue
- Cells
- Publisher
- MDPI AG
- Published
- 2020-07-24
- Volume
- 9
- Issue
- 8
- Pages
- 1773
- ISSN
- 2073-4409 (ISSN-L)
- PMC
- PMC7465464
- OpenAlex
- W3044845587
- Cited by
- 202
- References
- 114
- Citations by year
- 2026: 23 · 2025: 56 · 2024: 39 · 2023: 33 · 2022: 34 · 2021: 13 · 2020: 4
- FWCI
- 2.01
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cells (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Research Foundation of Korea (2020R1A6A1A03044512, NRF-2018R1A2B6001020)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Physical Performance
- Keywords
- insulin-like growth factor I, skeletal muscle, IGF-1 receptor, PI3K/Akt signaling, satellite cells, myogenesis, muscle mass, muscle strength, muscle degeneration, mechanical loading, Duchenne muscular dystrophy, muscle atrophy, neurite development, myoblast proliferation
- MeSH terms
- Cell Differentiation, Humans, Insulin-Like Growth Factor I, Muscle, Skeletal, Muscle Development
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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