{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T07:04:59Z","timestamp":1779433499911,"version":"3.53.1"},"reference-count":62,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T00:00:00Z","timestamp":1779408000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell Dev. Biol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      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\n                      <jats:sup>+<\/jats:sup>\n                      cells exhibited enriched inflammatory pathways and suppressed metabolic processes. In mdx mice, miR-30c-5p expression showed a pronounced reduction (P &amp;lt; 0.001). In contrast, SOCS3 expression increased at both the transcriptional (P &amp;lt; 0.001) and translational (P &amp;lt; 0.01) levels. Functional experiments further showed that overexpression of miR-30c-5p reduced SOCS3 expression, whereas inhibition of miR-30c-5p increased SOCS3 levels in C2C12 cells and primary skeletal muscle cells. Dual-luciferase reporter assay further supported direct binding of miR-30c-5p to the SOCS3 3\u2032UTR. In mdx-derived primary skeletal muscle cells, miR-30c-5p restoration was also accompanied by reduced TNF-\u03b1 and increased IL-10 levels, and rescue experiments supported that these anti-inflammatory effects were at least partly SOCS3-dependent.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These findings suggest that the miR-30c-5p\/SOCS3 axis is associated with inflammation- and metabolism-related alterations in DMD and warrants further investigation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcell.2026.1841851","type":"journal-article","created":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T06:08:48Z","timestamp":1779430128000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["The miR-30c-5p\/SOCS3 axis is a potential driver of inflammation and metabolic imbalance in Duchenne muscular dystrophy"],"prefix":"10.3389","volume":"14","author":[{"given":"Yayu","family":"Wang","sequence":"first","affiliation":[{"name":"School of Clinical Medicine, Qinghai University","place":["Xining, Qinghai, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiuyi","family":"Ai","sequence":"additional","affiliation":[{"name":"School of Clinical Medicine, Qinghai University","place":["Xining, Qinghai, China"]},{"name":"Department of Neurology, First Medical Center of Chinese PLA General Hospital","place":["Beijing, China"]},{"name":"Center for Translational Genomics and Rare Diseases, First Medical Center of Chinese PLA General Hospital","place":["Beijing, China"]},{"name":"Beijing Key Laboratory of Gene Editing Therapy for Hereditary Neuromuscular Diseases","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yue","family":"Chang","sequence":"additional","affiliation":[{"name":"School of Clinical Medicine, Qinghai University","place":["Xining, Qinghai, China"]},{"name":"Department of Neurology, First Medical Center of Chinese PLA General Hospital","place":["Beijing, China"]},{"name":"Center for Translational Genomics and Rare Diseases, First Medical Center of Chinese PLA General Hospital","place":["Beijing, China"]},{"name":"Beijing Key Laboratory of Gene Editing Therapy for Hereditary Neuromuscular Diseases","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shu","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Neurology, First Medical Center of Chinese PLA General Hospital","place":["Beijing, China"]},{"name":"Center for Translational Genomics and Rare Diseases, First Medical Center of Chinese PLA General Hospital","place":["Beijing, China"]},{"name":"Beijing Key Laboratory of Gene Editing Therapy for Hereditary Neuromuscular Diseases","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Neurology, First Medical Center of Chinese PLA General Hospital","place":["Beijing, China"]},{"name":"Center for Translational Genomics and Rare Diseases, First Medical Center of Chinese PLA General Hospital","place":["Beijing, China"]},{"name":"Beijing Key Laboratory of Gene Editing Therapy for Hereditary Neuromuscular Diseases","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shiwen","family":"Wu","sequence":"additional","affiliation":[{"name":"School of Clinical Medicine, Qinghai University","place":["Xining, Qinghai, China"]},{"name":"Department of Neurology, First Medical Center of Chinese PLA General Hospital","place":["Beijing, China"]},{"name":"Center for Translational Genomics and Rare Diseases, First Medical Center of Chinese PLA General Hospital","place":["Beijing, China"]},{"name":"Beijing Key Laboratory of Gene Editing Therapy for Hereditary Neuromuscular Diseases","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,5,22]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"C209","DOI":"10.1152\/ajpcell.00193.2016","article-title":"Muscle-specific microRNA-206 targets multiple components in dystrophic skeletal muscle representing beneficial adaptations","volume":"312","author":"Amirouche","year":"2017","journal-title":"Am. 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