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Molecular Research on Skeletal Muscle Metabolism and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 January 2026 | Viewed by 846

Special Issue Editor


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Guest Editor
Department of Life Sciences, National Central University, Jhongli 32001, Taiwan
Interests: autophagy; muscle development; muscle metabolism

Special Issue Information

Dear Colleagues,

Skeletal muscle (SKM) allows animals to move and perform various tasks and also plays critical roles in the regulation of systemic metabolism. About 35% of human body mass is occupied by SKM, which makes SKM the largest metabolic organ. So, maintaining normal SKM metabolic function is not only important to the performance of various tasks and ambulation but also to the systemic metabolism. Consequently, defective SKM metabolism will certainly have a drastic negative impact on SKM and various organs due to its systemic effect. In this Special Issue of IJMS, we cordially invite studies focusing on increasing our understanding of SKM metabolism and the diseases caused by its dysfunction. Both review and research articles addressing the following topics, but not limited to them, are welcome:

  1. Sarcopenia;
  2. Mitochondria and peroxisome homeostasis and function;
  3. Cachexia caused by cancer and chronic diseases;
  4. Stem cell renewal and differentiation in normal and diseased SKM;
  5. Myokines in systemic metabolism;
  6. Roles of immune cells in SKM diseases.

Prof. Dr. Shen-Liang Chen
Guest Editor

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Keywords

  • muscle
  • metabolism
  • mitochondria
  • peroxisome
  • stem cell
  • cahcexia

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Published Papers (1 paper)

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Research

16 pages, 2189 KB  
Article
Electronic Cigarette Exposure Induces Adverse Cellular Alterations in Skeletal Muscle in Male Mice Subjected to a High-Fat Diet
by Juan Carlos Rivera, Jorge Espinoza-Derout, Kamrul Hasan, Candice J. Lao, Julian Wilson, Yin Tintut, Xuesi M. Shao, Maria C. Jordan, Kenneth P. Roos, Yanjun Liu, Amiya P. Sinha-Hikim, Vishwajeet Puri and Theodore C. Friedman
Int. J. Mol. Sci. 2025, 26(23), 11491; https://doi.org/10.3390/ijms262311491 - 27 Nov 2025
Viewed by 253
Abstract
Electronic cigarettes (E-Cig) are a new way of delivering nicotine, gaining popularity among adolescents and young adults, who often do not realize their harmful effects. Although the adverse effects of E-Cigs on the liver and heart have been demonstrated, their effects on the [...] Read more.
Electronic cigarettes (E-Cig) are a new way of delivering nicotine, gaining popularity among adolescents and young adults, who often do not realize their harmful effects. Although the adverse effects of E-Cigs on the liver and heart have been demonstrated, their effects on the skeletal muscle have not been well studied. In this study, we evaluated the skeletal muscle effects of E-Cig aerosol, delivered in a manner similar to human vaping, in a mouse model of obesity induced by a high-fat diet (HFD). C57BL/6 mice, fed either a normal chow diet (NCD) or HFD, were exposed to either saline aerosol control or aerosol generated from Blu PLUSTM containing 0% or 2.4% nicotine for 12 weeks. Mice fed an NCD were included to distinguish whether E-Cig effects on the skeletal muscle required the presence of obesity induced by an HFD. The soleus muscle, an oxidative muscle rich in mitochondria, was assessed by Western blotting, electron microscopy, and biochemical assays. An NCD group was included to assess the baseline effects of HFD-induced obesity, on the skeletal muscle. The skeletal muscle from HFD-fed mice exposed to E-Cig 2.4% had reduced levels of phospho-AMPK compared with saline and E-Cig 0% groups, while E-Cigs had no effect on NCD-fed mice. Levels of phospho-adipose triglyceride lipase were also reduced in both E-Cig 2.4% and 0% compared with the saline group. These metabolic protein impairments were accompanied by increased levels of oxidative stress and phospho-p38 MAPK. Deregulation of the autophagy markers, microtubule-associated protein 1A/1B-light chain 3 (LC3-I; inactive form) and LC3-II (active form), was also observed, evidenced by decreased levels of LC3-II, ratio LC3-II/LC3-I, and increased levels of p62. Transmission electron microscopy analysis showed that E-Cig 2.4% induced damage to mitochondrial structure compared with the saline or E-Cig 0% groups. These findings suggest that E-Cig exposure on HFD impairs the skeletal muscle, adding to the growing list of affected organs for ongoing regulatory efforts concerning nicotine-containing substances. Full article
(This article belongs to the Special Issue Molecular Research on Skeletal Muscle Metabolism and Diseases)
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