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Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment—2nd Edition
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Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment—2nd Edition

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: closed (30 April 2025) | Viewed by 1763

Special Issue Editor

Dr. Andrea Telek

E-Mail Website
Guest Editor
Department of Physiology, University of Debrecen, Debrecen, Hungary
Interests: skeletal muscle
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will focus on the most recent findings on molecular advances in skeletal muscle function. Despite recent improvements in this field, important information is still missing regarding skeletal muscle metabolism. Mitochondria serve as the final targets of metabolism-related signalization pathways, and their dynamic nature requires precise regulatory mechanisms. A final response could be modified by epigenetic mechanisms, including the inhibition of protein translation by miRNA and other forms of gene expression regulation. Since skeletal muscle is involved in lipid and glucose homeostasis, it can serve as a target in the treatment of metabolic disorders. Additionally, understanding the molecular background of disorders primarily affecting skeletal muscle could improve therapeutic options in dystrophies, age-related muscle atrophy, and sarcopenia. In summary, further research is needed in order to completely understand the molecular regulation of skeletal muscle function. Therefore, we kindly invite you to publish your results in this Special Issue of IJMS entitled “Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment”. Submissions of original research papers and reviews are encouraged.

Dr. Andrea Telek
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.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • skeletal muscle
  • metabolism
  • mitochondria
  • epigenetics
  • exercise
  • signalization

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Related Special Issue

Published Papers (2 papers)

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Research

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20 pages, 3972 KiB  
Article
Myotube Formation and Cellular Fusion Are Diminished Due to Low Birth Weight in Piglets
by Katja Stange and Monika Röntgen
Int. J. Mol. Sci. 2025, 26(7), 2847; https://doi.org/10.3390/ijms26072847 - 21 Mar 2025
Viewed by 198
Abstract
Low birth weight (LBW) in various species leads to a pronounced skeletal muscle phenotype and can serve as a model to study muscle formation and draw conclusions for normal and pathological development. We aimed to elucidate in detail how the differentiation of muscular [...] Read more.
Low birth weight (LBW) in various species leads to a pronounced skeletal muscle phenotype and can serve as a model to study muscle formation and draw conclusions for normal and pathological development. We aimed to elucidate in detail how the differentiation of muscular stem cells and their progeny are disturbed in piglets born with LBW. We isolated primary muscle cells from LBW piglets and their normal siblings with two different approaches: (1) single cells from two functionally divergent subpopulations (previously named “fast” and “slow”) and (2) cells derived from isolated, intact myofibers. Subsequently, we analyzed their proliferative and differentiative capacity by determining proliferation rate, migration behavior, myotube formation, and myogenic gene and protein expression. LBW led to a decreased proliferation rate and migration potential in cells from the subpopulation fast group. Cells from LBW piglets were generally able to differentiate, but they formed smaller myotubes with less incorporated nuclei, leading to a diminished fusion rate. Myogenic gene expression was also significantly altered due to pig birth weight. Overall, early postnatal muscle development in LBW was disturbed at several crucial steps involving the establishment of a reserve stem cell pool, movement of cells towards existing myofibers, and the ability to form nascent myofibers. Full article
(This article belongs to the Special Issue Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment—2nd Edition)
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17 pages, 1097 KiB  
Opinion
Delayed-Onset Muscle Soreness Begins with a Transient Neural Switch
by Balázs Sonkodi
Int. J. Mol. Sci. 2025, 26(5), 2319; https://doi.org/10.3390/ijms26052319 - 5 Mar 2025
Viewed by 1226
Abstract
Unaccustomed and/or strenuous eccentric contractions are known to cause delayed-onset muscle soreness. In spite of this fact, their exact cause and mechanism have been unknown for more than 120 years. The exploration of the diverse functionality of the Piezo2 ion channel, as the [...] Read more.
Unaccustomed and/or strenuous eccentric contractions are known to cause delayed-onset muscle soreness. In spite of this fact, their exact cause and mechanism have been unknown for more than 120 years. The exploration of the diverse functionality of the Piezo2 ion channel, as the principal proprioceptive component, and its autonomously acquired channelopathy may bring light to this apparently simple but mysterious pain condition. Correspondingly, the neurocentric non-contact acute compression axonopathy theory of delayed-onset muscle soreness suggests two damage phases affecting two muscle compartments, including the intrafusal (within the muscle spindle) and the extrafusal (outside the muscle spindle) ones. The secondary damage phase in the extrafusal muscle space is relatively well explored. However, the suggested primary damage phase within the muscle spindle is far from being entirely known. The current manuscript describes how the proposed autonomously acquired Piezo2 channelopathy-induced primary damage could be the initiating transient neural switch in the unfolding of delayed-onset muscle soreness. This primary damage results in a transient proprioceptive neural switch and in a switch from quantum mechanical free energy-stimulated ultrafast proton-coupled signaling to rapid glutamate-based signaling along the muscle–brain axis. In addition, it induces a transient metabolic switch or, even more importantly, an energy generation switch in Type Ia proprioceptive terminals that eventually leads to a transient glutaminolysis deficit and mitochondrial deficiency, not to mention a force generation switch. In summary, the primary damage or switch is likely an inward unidirectional proton pathway reversal between Piezo2 and its auxiliary ligands, leading to acquired Piezo2 channelopathy. Full article
(This article belongs to the Special Issue Skeletal Muscle Function and Metabolism: Molecular Mechanisms and Treatment—2nd Edition)
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