ArticleExperimental and therapeutic medicine2021
Role of miRNAs and lncRNAs in dexamethasone-induced myotube atrophy
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- MyomiR Networks in Spinal Muscular Atrophy: Associations With Clinical Severity and Treatment Response.Molecular neurobiology · 2026Article
- Porcine Skeletal Muscle-Specific lncRNA-ssc.37456 Regulates Myoblast Proliferation and Differentiation.Animals : an open access journal from MDPI · 2026Article
- Comprehensive profiling of chemokine and NETosis-associated genes in sarcopenia: construction of a machine learning-based diagnostic nomogram.Frontiers in medicine · 2025Article
- Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024Review
- Morpho-Functional Analyses Demonstrate That Tyrosol Rescues Dexamethasone-Induced Muscle Atrophy.Journal of functional morphology and kinesiology · 2024Article
- Circulating myomiRNAs as biomarkers in patients with Cushing's syndrome.Journal of endocrinological investigation · 2024Article
- Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle atrophy is a well-known adverse effect of long-term glucocorticoid (GC) therapy. MicroRNAs (miRNAs or miRs) and long non-coding RNAs (lncRNAs) are important regulators in a number of physiological and pathological processes. However, the role of miRNAs and lncRNAs in the regulation of GC-treated muscle atrophy remains poorly understood. In the current study, muscular atrophy was induced and the results indicated that C2C12 myotubes were thinner than normal, while the expression of muscle ring finger protein 1 and Atrogin-1 was increased. The expression of nine miRNAs and seven lncRNAs associated with proliferation and differentiation were analyzed in a dexamethasone (DEX)-induced muscle atrophy cell model. In addition, the mRNA expression of the downstream targets of lncRNAs that were differentially expressed between DEX-treated and control cells were determined. The results indicated that the expression of miR-133a, miR-133b, miR-206 and five lncRNAs (increased Atrolnc-1, Dum, MAR1, linc-MD1 and decreased Myolinc) were significantly different between the DEX and the control group. Furthermore, the relative mRNA expression of Wnt5a and MyoD was significantly different between the two groups. The results of the current study indicated that some important miRNAs and lncRNAs are associated with DEX-induced muscle atrophy and have the potential to be further developed as a diagnostic tool for this condition.
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