Exploring LncRNA-Mediated Mechanisms in Muscle Regulation and Their Implications for Duchenne Muscular Dystrophy

This review examines the role of long non-coding RNAs (lncRNAs) in muscle regulation, particularly concerning Duchenne Muscular Dystrophy (DMD), a genetic disorder marked by muscle degeneration due to dystrophin deficiencies. LncRNAs, which modulate gene expression without coding for proteins, significantly impact muscle growth, development, and atrophy. The study identifies specific lncRNAs, such as Xist, H19, Malat1, and lnc-31, as key regulators of muscle degeneration and fibrosis, influencing pathways like PI3K/Akt and nitric oxide synthase signaling. These lncRNAs can modulate gene expression, affecting muscle differentiation and atrophy, with potential therapeutic benefits for DMD by enhancing muscle differentiation and reducing inflammation. The research underscores the complex interplay between lncRNAs, miRNAs, and gene networks in muscle pathology and regeneration, suggesting that manipulating lncRNA levels could offer new treatment strategies for DMD.