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DOI 10.3390/ijms26136032

Медицинская библиотека · International journal of molecular sciences · 2025

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

Gorji Abdolvahab Ebrahimpour, Roudbari Zahra, Ahmadian Kasra, Razban Vahid, Shirali Masoud, Hasanpur Karim, Sadkowski Tomasz

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Аннотация

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.

Для цитирования: Gorji Abdolvahab Ebrahimpour, Roudbari Zahra, Ahmadian Kasra, Razban Vahid, Shirali Masoud, Hasanpur Karim, Sadkowski Tomasz. Exploring lncRNA-Mediated Mechanisms in Muscle Regulation and Their Implications for Duchenne Muscular Dystrophy.. International journal of molecular sciences. 2025. DOI: 10.3390/ijms26136032.

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