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

Abstract

Duchenne muscular dystrophy (DMD) manifests as a hereditary condition that diminishes muscular strength through the progressive degeneration of structural muscle tissue, which is brought about by deficiencies in the dystrophin protein required for the integrity of muscle cells. DMD is among four different types of dystrophinopathy disorders. Current studies have established that long non-coding RNAs (lncRNAs) play a significant role in determining the trajectory and overall prognosis of chronic musculoskeletal conditions. LncRNAs are different in terms of their lengths, production mechanisms, and operational modes, but they do not produce proteins, as their primary activity is the regulation of gene expression. This research synthesizes current literature on the role of lncRNAs in the regulation of myogenesis with a specific focus on certain lncRNAs leading to DMD increments or suppressing muscle biological functions. LncRNAs modulate skeletal myogenesis gene expression, yet pathological lncRNA function is linked to various muscular diseases. Some lncRNAs directly control genes or indirectly control miRNAs with positive or negative effects on muscle cells or the development of DMD. The research findings have significantly advanced our knowledge about the regulatory function of lncRNAs on muscle growth and regeneration processes and DMD diseases.

Keywords: DMD; LncRNA; gene regulation; skeletal muscle.

Figure 1

Interactions of lncRNAs and miRNAs in the context of DMD (Pathway Studio Mammalian Web). Blue markers indicate lncRNAs that, together with miRNAs, are involved in interactions with disease-related genes.

Figure 2

The interaction of lncRNAs with hub genes.

Figure 3

A network diagram illustrating the interactions among miRNAs (pink), genes (green), and lncRNAs (blue), as well as their associations with key biological processes and pathways (orange) (Cytoscape software 3.10.3).