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Recent Advances in Skeletal Muscle Physiology and Pathophysiology

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 (31 January 2024) | Viewed by 5766

Special Issue Editor

Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), INSERM UMR-1297, Université Paul Sabatier, F-31432 Toulouse, Cedex, France
Interests: skeletal muscle; phosphoinositide metabolism; skeletal muscle proteoastasis; mtorc1 signalling; ubiquitin proteasome system

Special Issue Information

Dear Colleagues,

Skeletal muscle is the largest muscle in the human body, most are voluntarily controlled by the nerve system. The muscle cells of skeletal muscle, myofibrils, are composed of myofilaments, which in turn are composed of actin and myosin filaments. When action potentials travel along the cell membrane and carry the signal to the interior of the muscle fiber, thus initiate the contraction. The energy used for contracts are generated through the cleavage of ATP to ADP and inorganic phosphate, and also stored in short-term in the form of creatine phosphate.

To understand the skeleton muscle from the cellular and molecular level to integrated behavior, this special issue welcomes studies of biophysical and biochemical processes, homeostatic control mechanisms, and communication between cells that provide new insights into the underlying mechanisms. Articles about the role of actin and myosin in human health and disease are of particular interest.

Dr. Karim Hnia
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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Published Papers (3 papers)

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Research

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23 pages, 2480 KiB  
Article
The Acute, Short-, and Long-Term Effects of Endurance Exercise on Skeletal Muscle Transcriptome Profiles
by Thomas Beiter, Martina Zügel, Jens Hudemann, Marius Schild, Annunziata Fragasso, Christof Burgstahler, Karsten Krüger, Frank C. Mooren, Jürgen M. Steinacker and Andreas M. Nieß
Int. J. Mol. Sci. 2024, 25(5), 2881; https://doi.org/10.3390/ijms25052881 - 01 Mar 2024
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Abstract
A better understanding of the cellular and molecular mechanisms that are involved in skeletal muscle adaptation to exercise is fundamentally important to take full advantage of the enormous benefits that exercise training offers in disease prevention and therapy. The aim of this study [...] Read more.
A better understanding of the cellular and molecular mechanisms that are involved in skeletal muscle adaptation to exercise is fundamentally important to take full advantage of the enormous benefits that exercise training offers in disease prevention and therapy. The aim of this study was to elucidate the transcriptional signatures that distinguish the endurance-trained and untrained muscles in young adult males (24 ± 3.5 years). We characterized baseline differences as well as acute exercise-induced transcriptome responses in vastus lateralis biopsy specimens of endurance-trained athletes (ET; n = 8; VO2max, 67.2 ± 8.9 mL/min/kg) and sedentary healthy volunteers (SED; n = 8; VO2max, 40.3 ± 7.6 mL/min/kg) using microarray technology. A second cohort of SED volunteers (SED-T; n = 10) followed an 8-week endurance training program to assess expression changes of selected marker genes in the course of skeletal muscle adaptation. We deciphered differential baseline signatures that reflected major differences in the oxidative and metabolic capacity of the endurance-trained and untrained muscles. SED-T individuals in the training group displayed an up-regulation of nodal regulators of oxidative adaptation after 3 weeks of training and a significant shift toward the ET signature after 8 weeks. Transcriptome changes provoked by 1 h of intense cycling exercise only poorly overlapped with the genes that constituted the differential baseline signature of ETs and SEDs. Overall, acute exercise-induced transcriptional responses were connected to pathways of contractile, oxidative, and inflammatory stress and revealed a complex and highly regulated framework of interwoven signaling cascades to cope with exercise-provoked homeostatic challenges. While temporal transcriptional programs that were activated in SEDs and ETs were quite similar, the quantitative divergence in the acute response transcriptomes implicated divergent kinetics of gene induction and repression following an acute bout of exercise. Together, our results provide an extensive examination of the transcriptional framework that underlies skeletal muscle plasticity. Full article
(This article belongs to the Special Issue Recent Advances in Skeletal Muscle Physiology and Pathophysiology)
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15 pages, 6311 KiB  
Article
Skeletal Muscle-Specific Bis Depletion Leads to Muscle Dysfunction and Early Death Accompanied by Impairment in Protein Quality Control
by Soon-Young Jung, Tae-Ryong Riew, Hye Hyeon Yun, Ji Hee Lim, Ji-Won Hwang, Sung Won Jung, Hong Lim Kim, Jae-Seon Lee, Mun-Yong Lee and Jeong-Hwa Lee
Int. J. Mol. Sci. 2023, 24(11), 9635; https://doi.org/10.3390/ijms24119635 - 01 Jun 2023
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Abstract
Bcl-2-interacting cell death suppressor (BIS), also called BAG3, plays a role in physiological functions such as anti-apoptosis, cell proliferation, autophagy, and senescence. Whole-body Bis-knockout (KO) mice exhibit early lethality accompanied by abnormalities in cardiac and skeletal muscles, suggesting the critical role of [...] Read more.
Bcl-2-interacting cell death suppressor (BIS), also called BAG3, plays a role in physiological functions such as anti-apoptosis, cell proliferation, autophagy, and senescence. Whole-body Bis-knockout (KO) mice exhibit early lethality accompanied by abnormalities in cardiac and skeletal muscles, suggesting the critical role of BIS in these muscles. In this study, we generated skeletal muscle-specific Bis-knockout (Bis-SMKO) mice for the first time. Bis-SMKO mice exhibit growth retardation, kyphosis, a lack of peripheral fat, and respiratory failure, ultimately leading to early death. Regenerating fibers and increased intensity in cleaved PARP1 immunostaining were observed in the diaphragm of Bis-SMKO mice, indicating considerable muscle degeneration. Through electron microscopy analysis, we observed myofibrillar disruption, degenerated mitochondria, and autophagic vacuoles in the Bis-SMKO diaphragm. Specifically, autophagy was impaired, and heat shock proteins (HSPs), such as HSPB5 and HSP70, and z-disk proteins, including filamin C and desmin, accumulated in Bis-SMKO skeletal muscles. We also found metabolic impairments, including decreased ATP levels and lactate dehydrogenase (LDH) and creatine kinase (CK) activities in the diaphragm of Bis-SMKO mice. Our findings highlight that BIS is critical for protein homeostasis and energy metabolism in skeletal muscles, suggesting that Bis-SMKO mice could be used as a therapeutic strategy for myopathies and to elucidate the molecular function of BIS in skeletal muscle physiology. Full article
(This article belongs to the Special Issue Recent Advances in Skeletal Muscle Physiology and Pathophysiology)
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Review

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28 pages, 1422 KiB  
Review
Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting
by Pauline Henrot, Isabelle Dupin, Pierre Schilfarth, Pauline Esteves, Léo Blervaque, Maéva Zysman, Fares Gouzi, Maurice Hayot, Pascal Pomiès and Patrick Berger
Int. J. Mol. Sci. 2023, 24(7), 6454; https://doi.org/10.3390/ijms24076454 - 29 Mar 2023
Cited by 7 | Viewed by 2881
Abstract
Chronic obstructive pulmonary disease (COPD) is a worldwide prevalent respiratory disease mainly caused by tobacco smoke exposure. COPD is now considered as a systemic disease with several comorbidities. Among them, skeletal muscle dysfunction affects around 20% of COPD patients and is associated with [...] Read more.
Chronic obstructive pulmonary disease (COPD) is a worldwide prevalent respiratory disease mainly caused by tobacco smoke exposure. COPD is now considered as a systemic disease with several comorbidities. Among them, skeletal muscle dysfunction affects around 20% of COPD patients and is associated with higher morbidity and mortality. Although the histological alterations are well characterized, including myofiber atrophy, a decreased proportion of slow-twitch myofibers, and a decreased capillarization and oxidative phosphorylation capacity, the molecular basis for muscle atrophy is complex and remains partly unknown. Major difficulties lie in patient heterogeneity, accessing patients’ samples, and complex multifactorial process including extrinsic mechanisms, such as tobacco smoke or disuse, and intrinsic mechanisms, such as oxidative stress, hypoxia, or systemic inflammation. Muscle wasting is also a highly dynamic process whose investigation is hampered by the differential protein regulation according to the stage of atrophy. In this review, we report and discuss recent data regarding the molecular alterations in COPD leading to impaired muscle mass, including inflammation, hypoxia and hypercapnia, mitochondrial dysfunction, diverse metabolic changes such as oxidative and nitrosative stress and genetic and epigenetic modifications, all leading to an impaired anabolic/catabolic balance in the myocyte. We recapitulate data concerning skeletal muscle dysfunction obtained in the different rodent models of COPD. Finally, we propose several pathways that should be investigated in COPD skeletal muscle dysfunction in the future. Full article
(This article belongs to the Special Issue Recent Advances in Skeletal Muscle Physiology and Pathophysiology)
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