ArticleProceedings of the National Academy of Sciences of the United States of America2015
Glucocorticoids enhance muscle endurance and ameliorate Duchenne muscular dystrophy through a defined metabolic program.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- A Decade of Progress in Gene Targeted Therapeutic Strategies in Duchenne Muscular Dystrophy: A Systematic Review.Frontiers in bioengineering and biotechnology · 2022Pooled it
- Muscular response to the first three months of deflazacort treatment in boys with Duchenne muscular dystrophy.Journal of musculoskeletal & neuronal interactions · 2017Trial
- Regimen-dependent glucocorticoid effects improve muscle performance without altering CNS physiology in mdx mice.The Journal of physiology · 2026Article
- Targeting nuclear receptors in muscular dystrophies and regenerative myogenesis.Frontiers in cell and developmental biology · 2026Review
- Benefits of Steroid Injections into Paraspinous Muscles After Spinal Surgery in a Rat Paraspinal Muscle Retraction Model.International journal of molecular sciences · 2025Article
- Klf9 Loss of Function Protects Against Glucocorticoids Induced Skeletal Muscle Wasting.Journal of cachexia, sarcopenia and muscle · 2025Article
- FNDC1 is a myokine that promotes myogenesis and muscle regeneration.The EMBO journal · 2025Article
- Contractile regulation of the glucocorticoid-sensitive transcriptome in young and aged skeletal muscle.American journal of physiology. Endocrinology and metabolism · 2024Article
- The role of BCAA metabolism in metabolic health and disease.Experimental & molecular medicine · 2024Review
- A transcriptomics-based drug repositioning approach to identify drugs with similar activities for the treatment of muscle pathologies in spinal muscular atrophy (SMA) models.Human molecular genetics · 2024Article
- The transcriptional regulator KLF15 is necessary for myoblast differentiation and muscle regeneration by activating FKBP5.The Journal of biological chemistry · 2023Article
- Macrophagic AMPKα1 orchestrates regenerative inflammation induced by glucocorticoids.EMBO reports · 2023Article
- Protective Effect of Delta-Like 1 Homolog Against Muscular Atrophy in a Mouse Model.Endocrinology and metabolism (Seoul, Korea) · 2022Article
- Piezo1: opening the way to preventing muscle atrophy.The Journal of clinical investigation · 2022Article
- Synergistic Effects of Multiple Factors Involved in COVID-19-dependent Muscle Loss.Aging and disease · 2022Article
- Intermittent glucocorticoid treatment enhances skeletal muscle performance through sexually dimorphic mechanisms.The Journal of clinical investigation · 2022Article
- KLF15 cistromes reveal a hepatocyte pathway governing plasma corticosteroid transport and systemic inflammation.Science advances · 2022Article
- Corticosteroid Receptors in Cardiac Health and Disease.Advances in experimental medicine and biology · 2022Article
- Sexual Dimorphism in Transcriptional and Functional Glucocorticoid Effects on Mouse Skeletal Muscle.Frontiers in endocrinology · 2022Article
- KLF15 overexpression in myocytes fails to ameliorate ALS-related pathology or extend the lifespan of SOD1G93A mice.Neurobiology of disease · 2022Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
Abstract
Classic physiology studies dating to the 1930s demonstrate that moderate or transient glucocorticoid (GC) exposure improves muscle performance. The ergogenic properties of GCs are further evidenced by their surreptitious use as doping agents by endurance athletes and poorly understood efficacy in Duchenne muscular dystrophy (DMD), a genetic muscle-wasting disease. A defined molecular basis underlying these performance-enhancing properties of GCs in skeletal muscle remains obscure. Here, we demonstrate that ergogenic effects of GCs are mediated by direct induction of the metabolic transcription factor KLF15, defining a downstream pathway distinct from that resulting in GC-related muscle atrophy. Furthermore, we establish that KLF15 deficiency exacerbates dystrophic severity and muscle GC-KLF15 signaling mediates salutary therapeutic effects in the mdx mouse model of DMD. Thus, although glucocorticoid receptor (GR)-mediated transactivation is often associated with muscle atrophy and other adverse effects of pharmacologic GC administration, our data define a distinct GR-induced gene regulatory pathway that contributes to therapeutic effects of GCs in DMD through proergogenic metabolic programming.
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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.