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Molecular and Cellular Mechanisms and the Pathophysiology of Skeletal Muscle...
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Molecular and Cellular Mechanisms and the Pathophysiology of Skeletal Muscle 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 2025 | Viewed by 1222

Special Issue Editor

Dr. Gaetano Vattemi

E-Mail Website
Guest Editor
Department of Neurosciences, Biomedicine and Movement Sciences, Section of Clinical Neurology, University of Verona, Piazzale L.A. Scuro 10, 37134 Verona, Italy
Interests: idiopathic inflammatory myopathies; sporadic inclusion body myositis (sIBM); protein aggregates myopathies; nuclear envelopathies; amyotrophic lateral sclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Skeletal muscle is one of the most extended organs in the human body and is characterized by an elaborate architecture of multinucleated contractile myofibers within a complex microenvironment that includes endothelial and immune cells, motor neurons, perivascular and connective tissue, and muscle stem cells.

Several disorders affect the structure and/or function of skeletal muscle and can be classified into two broad categories: genetically determined and acquired myopathies. Many of these diseases are still awaiting effective treatments because their pathological mechanisms are not well understood. Recent advances in biological knowledge and technologies, such as stem cell protocols and high-throughput platforms, are making the study of molecular and cellular dynamics in skeletal muscle possible at unprecedented depths.

This Special Issue will update the latest findings on the biomolecular and cellular processes underlying primary muscle diseases, with the aim of improving understanding of their pathophysiological mechanisms and finding potential drug targets. Original research articles, reviews, and short communications related to this topic are all welcome.

Dr. Gaetano Vattemi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • acquired muscle diseases
  • inherited muscle diseases
  • pathogenesis
  • molecular and cellular mechanisms
  • in vitro and in vivo models
  • treatment strategies

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Published Papers (1 paper)

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Research

22 pages, 7966 KiB  
Article
P38α MAPK Coordinates Mitochondrial Adaptation to Caloric Surplus in Skeletal Muscle
by Liron Waingerten-Kedem, Sharon Aviram, Achinoam Blau, Tony Hayek and Eyal Bengal
Int. J. Mol. Sci. 2024, 25(14), 7789; https://doi.org/10.3390/ijms25147789 - 16 Jul 2024
Viewed by 853
Abstract
Excessive calorie intake leads to mitochondrial overload and triggers metabolic inflexibility and insulin resistance. In this study, we examined how attenuated p38α activity affects glucose and fat metabolism in the skeletal muscles of mice on a high-fat diet (HFD). Mice exhibiting diminished p38α [...] Read more.
Excessive calorie intake leads to mitochondrial overload and triggers metabolic inflexibility and insulin resistance. In this study, we examined how attenuated p38α activity affects glucose and fat metabolism in the skeletal muscles of mice on a high-fat diet (HFD). Mice exhibiting diminished p38α activity (referred to as p38αAF) gained more weight and displayed elevated serum insulin levels, as well as a compromised response in the insulin tolerance test, compared to the control mice. Additionally, their skeletal muscle tissue manifested impaired insulin signaling, leading to resistance in insulin-mediated glucose uptake. Examination of muscle metabolites in p38αAF mice revealed lower levels of glycolytic intermediates and decreased levels of acyl-carnitine metabolites, suggesting reduced glycolysis and β-oxidation compared to the controls. Additionally, muscles of p38αAF mice exhibited severe abnormalities in their mitochondria. Analysis of myotubes derived from p38αAF mice revealed reduced mitochondrial respiratory capacity relative to the myotubes of the control mice. Furthermore, these myotubes showed decreased expression of Acetyl CoA Carboxylase 2 (ACC2), leading to increased fatty acid oxidation and diminished inhibitory phosphorylation of pyruvate dehydrogenase (PDH), which resulted in elevated mitochondrial pyruvate oxidation. The expected consequence of reduced mitochondrial respiratory function and uncontrolled nutrient oxidation observed in p38αAF myotubes mitochondrial overload and metabolic inflexibility. This scenario explains the increased likelihood of insulin resistance development in the muscles of p38αAF mice compared to the control mice on a high-fat diet. In summary, within skeletal muscles, p38α assumes a crucial role in orchestrating the mitochondrial adaptation to caloric surplus by promoting mitochondrial biogenesis and regulating the selective oxidation of nutrients, thereby preventing mitochondrial overload, metabolic inflexibility, and insulin resistance. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms and the Pathophysiology of Skeletal Muscle Diseases)
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