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• W2066872481 abstract "microRNAs (miRNAs) are noncoding RNAs that regulate gene expression in post-transcriptional fashion, and emerging studies support their importance in a multitude of physiological and pathological processes. Here, we describe the regulation and function of miR-29 in Duchenne muscular dystrophy (DMD) and its potential use as therapeutic target. Our results demonstrate that miR-29 expression is downregulated in dystrophic muscles of mdx mice, a model of DMD. Restoration of its expression by intramuscular and intravenous injection improved dystrophy pathology by both promoting regeneration and inhibiting fibrogenesis. Mechanistic studies revealed that loss of miR-29 in muscle precursor cells (myoblasts) promotes their transdifferentiation into myofibroblasts through targeting extracellular molecules including collagens and microfibrillar-associated protein 5 (Mfap5). We further demonstrated that miR-29 is under negative regulation by transforming growth factor-β (TGF-β) signaling. Together, these results not only identify TGF-β-miR-29 as a novel regulatory axis during myoblasts conversion into myofibroblasts which constitutes a novel contributing route to muscle fibrogenesis of DMD but also implicate miR-29 replacement therapy as a promising treatment approach for DMD." @default.
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• W2066872481 date "2012-06-01" @default.
• W2066872481 modified "2023-10-07" @default.
• W2066872481 title "Loss of miR-29 in Myoblasts Contributes to Dystrophic Muscle Pathogenesis" @default.
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• W2066872481 doi "https://doi.org/10.1038/mt.2012.35" @default.
• W2066872481 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3369280" @default.
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