Advances in Understanding Skeletal Muscle Metabolism and Regeneration: From Mechanisms to Therapeutics

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 617

Special Issue Editor


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Guest Editor
Department of Diagnostic and Health Sciences, College of Health Professions, The University of Tennessee Health Science Center, Memphis, TN, USA
Interests: aging; stroke; skeletal muscle atrophy, growth, regeneration, and metabolism; genomics; proteomics; metabolomics; bioinformatics
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Special Issue Information

Dear Colleagues,

Skeletal muscle, which accounts for 40% of total body weight, has diverse functions, including maintaining body posture and producing mobility and movement. Skeletal muscle is also essential for maintaining whole-body energy homeostasis, as it is involved in glucose and fatty acid metabolisms. Muscle tissue deteriorates with aging both quantitatively and qualitatively, which increases the risks of falls, osteoporosis, and metabolic diseases. Thus, maintaining muscle mass is important for a healthier life. Moreover, muscle mass can significantly impact the effects of various treatments, particularly in scenarios like cachexia, where a higher muscle mass often leads to better tolerance of treatment side effects and improved overall outcomes. In contrast, significant muscle loss (muscle wasting) can indicate poorer prognosis and increased toxicity due to reduced ability to withstand treatment stress; essentially, more muscle mass generally means better ability to cope with treatment demands. Therefore, maintaining muscle mass is important for whole-body metabolic homeostasis. Similarly, proper muscle regeneration is a key to maintaining muscle mass because it has been shown that muscle regeneration is significantly reduced in many disease and disorder conditions. We are looking for any kind of research manuscript that shows the data related to muscle metabolisms and regeneration.

Dr. Junaith S. Mohamed
Guest Editor

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Keywords

  • skeletal muscle
  • satellite cells
  • myoblast
  • myogenesis
  • regeneration
  • mitochondria
  • metabolism
  • sarcopenia
  • cachexia

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Published Papers (1 paper)

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Research

20 pages, 1740 KiB  
Article
Regulation of Myogenesis by MechanomiR-200c/FoxO3 Axis
by Junaith S. Mohamed and Aladin M. Boriek
Cells 2025, 14(12), 868; https://doi.org/10.3390/cells14120868 - 9 Jun 2025
Viewed by 281
Abstract
Cyclic mechanical stretch has been shown to inhibit myoblast differentiation while promoting proliferation. However, the underlying molecular mechanisms are not well understood. Here, we report that mechanical stretch inhibits the differentiation of mouse primary myoblasts by promoting the cell cycle program and by [...] Read more.
Cyclic mechanical stretch has been shown to inhibit myoblast differentiation while promoting proliferation. However, the underlying molecular mechanisms are not well understood. Here, we report that mechanical stretch inhibits the differentiation of mouse primary myoblasts by promoting the cell cycle program and by inhibiting the expression of the myogenic regulator MyoD. Stretch alters the miRNA expression profile as evidenced by miRNA microarray analysis. We identified miR-200c as one of the highly downregulated mechanosensitive miRNAs (mechanomiRs) whose expression level was increased during differentiation. This suggests that mechanomiRs-200c is a myogenic miRNA. Overexpression of mechanomiR-200c revoked the effect of stretch on myoblast differentiation, and the introduction of the mechanomiR-200c antagomir restored the stretch effect. This suggests that stretch blocks differentiation, in part, through mechanomiR-200c. The gene encoding the transcription factor FoxO3 is a known direct target of mechanomiR-200c. Interestingly, MyoD binds to the mechanomiR-200c promoter in differentiating myoblasts, whereas stretch appears to reverse such binding. Our data further demonstrate that the levels of mechanomiR-200c are robustly elevated during the early stage of the muscle repair process in young mice, but not in the injured muscle of aged mice. Overall, we identified a novel pathway, MyoD/mechanomiR-200c/FoxO3a, and the potential mechanism by which stretch inhibits myoblast differentiation. Full article
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