ArticleFrontiers in cell and developmental biology2026
The miR-30c-5p/SOCS3 axis is a potential driver of inflammation and metabolic imbalance in Duchenne muscular dystrophy.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Duchenne muscular dystrophy (DMD) constitutes a severe, incurable disorder inherited in an X-linked manner, characterized by continuous skeletal muscle degeneration, chronic inflammatory responses, and profound metabolic alterations. Although miRNA-mRNA regulatory networks are thought to contribute to DMD pathogenesis, their key drivers remain insufficiently defined. Methods: In this study, we integrated bulk RNA-seq (GSE38417, GSE109178), small RNA-seq (GSE157668), and single-cell RNA-seq (GSE213925) data and combined differential expression analysis, target gene prediction, functional pathway enrichment mapping, and protein-protein interaction network analysis to screen candidate miRNA-mRNA axes, which were subsequently validated in mdx mice, C2C12 myoblasts, and primary skeletal muscle cells. Results: We identified 100 differentially expressed miRNAs (DEMs) in DMD muscle, with miR-30c-5p being the most downregulated and possessing the highest number of predicted targets. Integrated analysis revealed SOCS3 as a key upregulated hub gene targeted by miR-30c-5p. ScRNA-seq showed elevated SOCS3 expression in myocytes from DMD muscle, where SOCS3 Conclusion: These findings suggest that the miR-30c-5p/SOCS3 axis is associated with inflammation- and metabolism-related alterations in DMD and warrants further investigation.
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