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Emerging Mechanisms for Skeletal Muscle Mass Regulation
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Emerging Mechanisms for Skeletal Muscle Mass Regulation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 16962

Special Issue Editors

Prof. Dr. Vincenzo Sorrentino

E-Mail Website
Guest Editor
Department of Molecular and Developmental Medicine, University of Siena, 53100 Siena, Italy
Interests: cellular and molecular muscle biology; myogenesis; genetics of muscle diseases; muscular dystrophy; excitation contraction coupling; malignant hyperthermia; molecular and cellular biology; skeletal muscle physiology; skeletal muscle metabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Stefano Perni

E-Mail Website
Guest Editor
Department of Physiology & Biophysics, University of Colorado Anschutz Medical Campus, 12800 E. 19th Ave, Aurora, CO 80045, USA
Interests: cellular and molecular muscle biology; skeletal muscle physiology; electrophysiology of excitation–contraction coupling; calcium signaling

Special Issue Information

Dear Colleagues,

Skeletal muscle makes up approximately 40% of the total human body mass and plays a key role in locomotion, breathing, posture and metabolism. Skeletal muscle mass is finely regulated in the healthy human body, but a significant and deleterious loss of skeletal muscle mass can occur as a consequence of pathological conditions such as cancer, chronic renal failure, AIDS, and multiple sclerosis. Additionally, a progressive reduction in muscle mass is almost invariably observed during aging. Regardless of its origin, severe loss of muscle mass leads to a significant decline in quality of life in terms of decreased independence, risks of injuries, hospitalization and even susceptibility to diseases. However, the mechanisms behind this pathological condition are not yet fully understood, and are likely multifactorial. The devastating, life-changing consequences of muscle loss, especially in young individuals, and the expected ever-growing price in terms of individual well-being and global health care costs of age-related muscle loss in a globally aging population, call for an effort from the scientific community to investigate and understand the molecular mechanisms underlying the regulation of muscle mass.

For this Special Issue, we invite both original research articles and reviews that provide the IJMS reader a comprehensive picture of recent advancements in the field of skeletal muscle mass regulation in terms of new exciting findings and cutting-edge methodologies possibly leading to new therapeutic strategies to improve the well-being of individuals affected by abnormal muscle mass regulation.

Prof. Dr. Vincenzo Sorrentino
Dr. Stefano Perni
Guest Editors

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

  • exercise and skeletal muscle
  • muscular dystrophies and myopathies
  • sarcopenia
  • cachexia
  • autophagy and atrophy
  • hypertrophy
  • insulin/IGF1 signaling
  • AKT, mTOR, AMPK pathways
  • myokines

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Published Papers (4 papers)

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Research

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17 pages, 6640 KiB  
Article
Reduced Expression of Septin7 Hinders Skeletal Muscle Regeneration
by László Szabó, Andrea Telek, János Fodor, Nóra Dobrosi, Klaudia Dócs, Zoltán Hegyi, Mónika Gönczi, László Csernoch and Beatrix Dienes
Int. J. Mol. Sci. 2023, 24(17), 13536; https://doi.org/10.3390/ijms241713536 - 31 Aug 2023
Cited by 2 | Viewed by 1576
Abstract
Septins are considered the fourth component of the cytoskeleton with the septin7 isoform playing a critical role in the formation of diffusion barriers in phospholipid bilayers and intra- and extracellular scaffolds. While its importance has already been confirmed in different intracellular processes, very [...] Read more.
Septins are considered the fourth component of the cytoskeleton with the septin7 isoform playing a critical role in the formation of diffusion barriers in phospholipid bilayers and intra- and extracellular scaffolds. While its importance has already been confirmed in different intracellular processes, very little is known about its role in skeletal muscle. Muscle regeneration was studied in a Sept7 conditional knock-down mouse model to prove the possible role of septin7 in this process. Sterile inflammation in skeletal muscle was induced which was followed by regeneration resulting in the upregulation of septin7 expression. Partial knock-down of Sept7 resulted in an increased number of inflammatory cells and myofibers containing central nuclei. Taken together, our data suggest that partial knock-down of Sept7 hinders the kinetics of muscle regeneration, indicating its crucial role in skeletal muscle functions. Full article
(This article belongs to the Special Issue Emerging Mechanisms for Skeletal Muscle Mass Regulation)
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16 pages, 3712 KiB  
Article
Muscle Regeneration in Holothurians without the Upregulation of Muscle Genes
by Vladimir A. Nizhnichenko, Alexey V. Boyko, Talia T. Ginanova and Igor Yu. Dolmatov
Int. J. Mol. Sci. 2022, 23(24), 16037; https://doi.org/10.3390/ijms232416037 - 16 Dec 2022
Cited by 3 | Viewed by 2534
Abstract
The holothurian Eupentacta fraudatrix is capable of fully restoring its muscles after transverse dissection. Although the regeneration of these structures is well studied at the cellular level, the molecular basis of the process remains poorly understood. To identify genes that may be involved [...] Read more.
The holothurian Eupentacta fraudatrix is capable of fully restoring its muscles after transverse dissection. Although the regeneration of these structures is well studied at the cellular level, the molecular basis of the process remains poorly understood. To identify genes that may be involved in the regulation of muscle regeneration, the transcriptome of the longitudinal muscle band of E. fraudatrix has been sequenced at different time periods post-injury. An analysis of the map of biological processes and pathways has shown that most genes associated with myogenesis decrease their expression during the regeneration. The only exception is the genes united by the GO term “heart valve development”. This may indicate the antiquity of mechanisms of mesodermal structure transformation, which was co-opted into various morphogeneses in deuterostomes. Two groups of genes that play a key role in the regeneration have been analyzed: transcription factors and matrix metalloproteinases. A total of six transcription factor genes (Ef-HOX5, Ef-ZEB2, Ef-RARB, Ef-RUNX1, Ef-SOX17, and Ef-ZNF318) and seven matrix metalloproteinase genes (Ef-MMP11, Ef-MMP13, Ef-MMP13-1, Ef-MMP16-2, Ef-MMP16-3, Ef-MMP24, and Ef-MMP24-1) showing differential expression during myogenesis have been revealed. The identified genes are assumed to be involved in the muscle regeneration in holothurians. Full article
(This article belongs to the Special Issue Emerging Mechanisms for Skeletal Muscle Mass Regulation)
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16 pages, 3227 KiB  
Article
Immunoproteasome Inhibition Ameliorates Aged Dystrophic Mouse Muscle Environment
by Luana Tripodi, Davide Molinaro, Francesco Fortunato, Carolina Mella, Barbara Cassani, Yvan Torrente and Andrea Farini
Int. J. Mol. Sci. 2022, 23(23), 14657; https://doi.org/10.3390/ijms232314657 - 24 Nov 2022
Cited by 5 | Viewed by 3137
Abstract
Muscle wasting is a major pathological feature observed in Duchenne muscular dystrophy (DMD) and is the result of the concerted effects of inflammation, oxidative stress and cell senescence. The inducible form of proteasome, or immunoproteasome (IP), is involved in all the above mentioned [...] Read more.
Muscle wasting is a major pathological feature observed in Duchenne muscular dystrophy (DMD) and is the result of the concerted effects of inflammation, oxidative stress and cell senescence. The inducible form of proteasome, or immunoproteasome (IP), is involved in all the above mentioned processes, regulating antigen presentation, cytokine production and immune cell response. IP inhibition has been previously shown to dampen the altered molecular, histological and functional features of 3-month-old mdx mice, the animal model for DMD. In this study, we described the role of ONX-0914, a selective inhibitor of the PSMB8 subunit of immunoproteasome, in ameliorating the pathological traits that could promote muscle wasting progression in older, 9-month-old mdx mice. ONX-0914 reduces the number of macrophages and effector memory T cells in muscle and spleen, while increasing the number of regulatory T cells. It modulates inflammatory markers both in skeletal and cardiac muscle, possibly counteracting heart remodeling and hypertrophy. Moreover, it buffers oxidative stress by improving mitochondrial efficiency. These changes ultimately lead to a marked decrease of fibrosis and, potentially, to more controlled myofiber degeneration/regeneration cycles. Therefore, ONX-0914 is a promising molecule that may slow down muscle mass loss, with relatively low side effects, in dystrophic patients with moderate to advanced disease. Full article
(This article belongs to the Special Issue Emerging Mechanisms for Skeletal Muscle Mass Regulation)
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Review

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20 pages, 1175 KiB  
Review
Sex Differences in Inflammation and Muscle Wasting in Aging and Disease
by Chiara Della Peruta, Biliana Lozanoska-Ochser, Alessandra Renzini, Viviana Moresi, Carles Sanchez Riera, Marina Bouché and Dario Coletti
Int. J. Mol. Sci. 2023, 24(5), 4651; https://doi.org/10.3390/ijms24054651 - 28 Feb 2023
Cited by 48 | Viewed by 8908
Abstract
Only in recent years, thanks to a precision medicine-based approach, have treatments tailored to the sex of each patient emerged in clinical trials. In this regard, both striated muscle tissues present significant differences between the two sexes, which may have important consequences for [...] Read more.
Only in recent years, thanks to a precision medicine-based approach, have treatments tailored to the sex of each patient emerged in clinical trials. In this regard, both striated muscle tissues present significant differences between the two sexes, which may have important consequences for diagnosis and therapy in aging and chronic illness. In fact, preservation of muscle mass in disease conditions correlates with survival; however, sex should be considered when protocols for the maintenance of muscle mass are designed. One obvious difference is that men have more muscle than women. Moreover, the two sexes differ in inflammation parameters, particularly in response to infection and disease. Therefore, unsurprisingly, men and women respond differently to therapies. In this review, we present an up-to-date overview on what is known about sex differences in skeletal muscle physiology and disfunction, such as disuse atrophy, age-related sarcopenia, and cachexia. In addition, we summarize sex differences in inflammation which may underly the aforementioned conditions because pro-inflammatory cytokines deeply affect muscle homeostasis. The comparison of these three conditions and their sex-related bases is interesting because different forms of muscle atrophy share common mechanisms; for instance, those responsible for protein dismantling are similar although differing in terms of kinetics, severity, and regulatory mechanisms. In pre-clinical research, exploring sexual dimorphism in disease conditions could highlight new efficacious treatments or recommend implementation of an existing one. Any protective factors discovered in one sex could be exploited to achieve lower morbidity, reduce the severity of the disease, or avoid mortality in the opposite sex. Thus, the understanding of sex-dependent responses to different forms of muscle atrophy and inflammation is of pivotal importance to design innovative, tailored, and efficient interventions. Full article
(This article belongs to the Special Issue Emerging Mechanisms for Skeletal Muscle Mass Regulation)
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