ArticleAmerican journal of physiology. Endocrinology and metabolism2012
A cell-autonomous role for the glucocorticoid receptor in skeletal muscle atrophy induced by systemic glucocorticoid exposure.
Article in American journal of physiology. Endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 119 citations in OpenAlex.
- Targeting nuclear receptors in muscular dystrophies and regenerative myogenesis.Frontiers in cell and developmental biology · 2026Review
- The skeletal muscle of aged male mice exhibits sustained growth regulatory transcriptional profile following glucocorticoid exposure compared with young males.Physiological genomics · 2025Article
- Short-term daily deflazacort decreases membrane permeability and increases maximum force inAmerican journal of physiology. Cell physiology · 2025Article
- Klf9 Loss of Function Protects Against Glucocorticoids Induced Skeletal Muscle Wasting.Journal of cachexia, sarcopenia and muscle · 2025Article
- Carnosine ameliorates dexamethasone-induced muscle atrophy with associated modulation of ubiquitin ligases and oxidative stress in C57BL/6J female mice.Current research in physiology · 2025Article
- Relationship between hemoglobin glycation index and Cushing's syndrome: a cross-sectional study in Chinese populations.Frontiers in endocrinology · 2025Article
- The role of oxidative stress, glucocorticoid receptor and ARMC5 in lipid metabolism.Endocrine journal · 2024Review
- The glucocorticoid receptor acts locally to protect dystrophic muscle and heart during disease.Disease models & mechanisms · 2024Article
- LSD1 inhibition circumvents glucocorticoid-induced muscle wasting of male mice.Nature communications · 2024Article
- FGF21 Induces Skeletal Muscle Atrophy and Increases Amino Acids in Female Mice: A Potential Role for Glucocorticoids.Endocrinology · 2024Article
- Functional annotation of regulatory elements in rainbow trout uncovers roles of the epigenome in genetic selection and genome evolution.GigaScience · 2024Article
- Lesion level-dependent systemic muscle wasting after spinal cord injury is mediated by glucocorticoid signaling in mice.Science translational medicine · 2023Article
- Class I HDAC inhibitors attenuate dexamethasone-induced muscle atrophy via increased protein kinase C (PKC) delta phosphorylation.Cellular signalling · 2023Article
- Protective Role of Ethanol Extract ofInternational journal of molecular sciences · 2023Article
- The crucial role of muscle glucocorticoid signaling in accelerating obesity and glucose intolerance via hyperinsulinemia.JCI insight · 2023Article
- Musculoskeletal complications of Cushing syndrome.Reumatologia · 2023Review
- Hypothalamic-pituitary-adrenal axis activation and glucocorticoid-responsive gene expression in skeletal muscle and liver of Apc mice.Journal of cachexia, sarcopenia and muscle · 2022Article
- Intermittent glucocorticoid treatment enhances skeletal muscle performance through sexually dimorphic mechanisms.The Journal of clinical investigation · 2022Article
- Current status of glucocorticoid usage in solid organ transplantation.World journal of transplantation · 2021Review
- Myod1 and GR coordinate myofiber-specific transcriptional enhancers.Nucleic acids research · 2021Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Glucocorticoids (GCs) are important regulators of skeletal muscle mass, and prolonged exposure will induce significant muscle atrophy. To better understand the mechanism of skeletal muscle atrophy induced by elevated GC levels, we examined three different models: exogenous synthetic GC treatment [dexamethasone (DEX)], nutritional deprivation, and denervation. Specifically, we tested the direct contribution of the glucocorticoid receptor (GR) in skeletal muscle atrophy by creating a muscle-specific GR-knockout mouse line (MGR(e3)KO) using Cre-lox technology. In MGR(e3)KO mice, we found that the GR is essential for muscle atrophy in response to high-dose DEX treatment. In addition, DEX regulation of multiple genes, including two important atrophy markers, MuRF1 and MAFbx, is eliminated completely in the MGR(e3)KO mice. In a condition where endogenous GCs are elevated, such as nutritional deprivation, induction of MuRF1 and MAFbx was inhibited, but not completely blocked, in MGR(e3)KO mice. In response to sciatic nerve lesion and hindlimb muscle denervation, muscle atrophy and upregulation of MuRF1 and MAFbx occurred to the same extent in both wild-type and MGR(e3)KO mice, indicating that a functional GR is not required to induce atrophy under these conditions. Therefore, we demonstrate conclusively that the GR is an important mediator of skeletal muscle atrophy and associated gene expression in response to exogenous synthetic GCs in vivo and that the MGR(e3)KO mouse is a useful model for studying the role of the GR and its target genes in multiple skeletal muscle atrophy models.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.