ArticleJournal of cachexia, sarcopenia and muscle2025
Klf9 Loss of Function Protects Against Glucocorticoids Induced Skeletal Muscle Wasting.
Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Loss of LCN2 Function Ameliorates Glucocorticoid-Induced Muscle Atrophy via Remodeling the Extracellular Matrix.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mechanistic interactions of diet, exercise, and pharmacotherapy in skeletal muscle metabolism: evidence and translational perspectives.Frontiers in physiology · 2026Review
- Comprehensive Identification of the Bovine KLF Gene Family and Its Functional Regulation in Muscle Development: Insights from Single-Nuclei Transcriptomics.Animals : an open access journal from MDPI · 2025Article
- Klf9 Loss of Function Protects Against Glucocorticoids Induced Skeletal Muscle Wasting.Journal of cachexia, sarcopenia and muscle · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundGlucocorticoids (GCs) are the most important and frequently used class of anti-inflammatory drugs. However, the mechanisms underlying excessive glucocorticoid-mediated induction of muscle atrophy remain incompletely understood.
methodsWe generated skeletal muscle-specific Klf9 transgenic mice (mKlf9TG) and skeletal muscle-specific Klf9 knockout mice (Klf9
resultsSkeletal muscle Klf9 gene expression was significantly upregulated by Dex (p < 0.05 or p < 0.01 vs. vehicle group). Compared with littermate control mice (R-loxP), mKlf9TG mice exhibited decreased skeletal muscle mass (TA 0.101 ± 0.018 vs. 0.040 ± 0.007 g, p < 0.001) and impaired grip strength (forelimb 157.4 ± 3.7 vs. 93.45 ± 9.8 and four limbs 255.3 ± 23.1 vs. 170.1 ± 36.2, p < 0.001). Conversely, compared with Klf9
conclusionsIn summary, our study provides novel insights into the mechanisms underlying GC-induced muscular atrophy and reveals that skeletal muscle induction of Klf9 expression is a mechanism underlying GC therapy-induced muscle loss. Thus, targeting Klf9 may offer novel approaches to the treatment of skeletal muscle wasting diseases.
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