Cited by 705Muscle Physiology and DisordersMuscle metabolism and nutritionNutrition and Health in Aging

The DOI matches its Crossref record; 155 of the 157 references it cites were found in a registry or an index.

Glucocorticoid-induced skeletal muscle atrophy

Schakman, O., Kalista, S., Barbé, C., Loumaye, A., Thissen, J.P.·2013·The International Journal of Biochemistry & Cell Biology

DOI 10.1016/j.biocel.2013.05.036

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Abstract

Many pathological states characterized by muscle atrophy (e.g., sepsis, cachexia, starvation, metabolic acidosis and severe insulinopenia) are associated with an increase in circulating glucocorticoids (GC) levels, suggesting that GC could trigger the muscle atrophy observed in these conditions. GC-induced muscle atrophy is characterized by fast-twitch, glycolytic muscles atrophy illustrated by decreased fiber cross-sectional area and reduced myofibrillar protein content. GC-induced muscle atrophy results from increased protein breakdown and decreased protein synthesis. Increased muscle proteolysis, in particular through the activation of the ubiquitin proteasome and the lysosomal systems, is considered to play a major role in the catabolic action of GC. The stimulation by GC of these two proteolytic systems is mediated through the increased expression of several Atrogenes ("genes involved in atrophy"), such as FOXO, Atrogin-1, and MuRF-1. The inhibitory effect of GC on muscle protein synthesis is thought to result mainly from the inhibition of the mTOR/S6 kinase 1 pathway. These changes in muscle protein turnover could be explained by changes in the muscle production of two growth factors, namely Insulin-like Growth Factor (IGF)-I, a muscle anabolic growth factor and Myostatin, a muscle catabolic growth factor. This review will discuss the recent progress made in the understanding of the mechanisms involved in GC-induced muscle atrophy and consider the implications of these advancements in the development of new therapeutic approaches for treating GC-induced myopathy. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.

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Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy.
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“…analyses of muscle atrophy due to a variety of wasting diseases are several genes (Atrogin-1, MuRF-1, Cathepsin-L, PDK4, p21, Gadd45, 4E-BP1) controlled by the FOXO transcription factors (Almon et al., 2007; Jagoe et al., 2002; Komamura et al., 2003; Lecker et al., 2004; Waddell et al., 2008).”
Background
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Authors: Schakman, O., Kalista, S., Barbé, C., Loumaye, A., & Thissen, J. P.
Affiliations: UCLouvain (BE)
Corresponding author: Thissen, J.P.
ORCID: Schakman, O.
Barbé, C.
Loumaye, A.
Venue: The International Journal of Biochemistry & Cell Biology
Publisher: Elsevier BV
Published: 2013-10
Volume: 45
Issue: 10
Pages: 2163-2172
ISSN: 1357-2725 (ISSN-L)
DOI: 10.1016/j.biocel.2013.05.036
OpenAlex: W2092885411
Cited by: 705
References: 157
Citations by year: 2026: 81 · 2025: 74 · 2024: 58 · 2023: 60 · 2022: 68 · 2021: 62 · 2020: 58 · 2019: 43 · 2018: 44 · 2017: 37 · 2016: 45 · 2015: 48 · 2014: 24 · 2013: 2
FWCI: 3.73
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: The International Journal of Biochemistry & Cell Biology (publishedVersion)
PubMed (publishedVersion)
Digital Access to Libraries (submittedVersion)
Funders: Fund for Scientific Medical Research (Belgium)
National Fund for Scientific Research (Belgium)
Association Française contre les Myopathies (France)
Association Belge contre les Maladies neuro-musculaires
Fonds Spéciaux de Recherche (Université catholique de Louvain, Belgium)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
Health Sciences › Medicine › Physiology (medical) › Nutrition and Health in Aging
Keywords: glucocorticoid-induced muscle atrophy, skeletal muscle atrophy, muscle protein degradation, ubiquitin-proteasome system, lysosomal proteolysis, atrogenes, atrogin-1, MuRF1, FOXO, muscle protein synthesis, insulin-like growth factor I, myostatin, glucocorticoid-induced myopathy, cachexia, sepsis
MeSH terms: Animals, Glucocorticoids, Humans, Muscular Atrophy, Protein Biosynthesis, Signal Transduction

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Glucocorticoid-induced skeletal muscle atrophy

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