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The Physiology of Striated Muscle Tissue 2.0
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The Physiology of Striated Muscle Tissue 2.0

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 August 2023) | Viewed by 7230

Special Issue Editor

Dr. Frank Suhr

E-Mail Website
Guest Editor
Division of Molecular Exercise Physiology, Faculty of Life Sciences: Food, Nutrition and Health, University of Bayreuth, 95447 Bayreuth, Germany
Interests: skeletal muscle; cardiac muscle; muscle physiology; exercise physiology; mechanosensing; metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to highlight recent and current research in the field of ‘The physiology of striated muscle tissues’. Striated muscle tissue comprises skeletal and cardiac muscles, both highly dynamic tissues responding and adapting to various stimuli (metabolic, environmental, mechanical, etc.). Furthermore, skeletal and cardiac muscles critically control whole-body metabolic homeostasis, reflected by the fact that skeletal muscles represent 40–50% of the body mass. In addition, striated muscle dysfunctions contribute to a wide spectrum of disease, including (but not limited to) cardiovascular diseases, metabolic syndrome, frailty, diabetes mellitus type 2, and muscular dystrophies. These examples demonstrate that striated muscles play key roles in the physiological homeostasis of the human body, whereas a slight aberrance from physiological control conditions causes or drives (severe) disease.

The core of this Special Issue is to assemble cutting-edge studies that use different experimental approaches in vivo (human and animal models) and/or in vitro to dissect the dynamic alterations of skeletal and cardiac muscles under healthy and diseased conditions.

Dr. Frank Suhr
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
  • cardiac muscle
  • health
  • disease
  • human/animal/cell culture
  • exercise
  • disease models

Related Special Issue

Published Papers (4 papers)

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Research

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20 pages, 12459 KiB  
Article
Human Mutated MYOT and CRYAB Genes Cause a Myopathic Phenotype in Zebrafish
by Elena Cannone, Valeria Guglielmi, Giulia Marchetto, Chiara Tobia, Barbara Gnutti, Barbara Cisterna, Paola Tonin, Alessandro Barbon, Gaetano Vattemi and Marco Schiavone
Int. J. Mol. Sci. 2023, 24(14), 11483; https://doi.org/10.3390/ijms241411483 - 14 Jul 2023
Viewed by 936
Abstract
Myofibrillar myopathies (MFMs) are a group of hereditary neuromuscular disorders sharing common histological features, such as myofibrillar derangement, Z-disk disintegration, and the accumulation of degradation products into protein aggregates. They are caused by mutations in several genes that encode either structural proteins or [...] Read more.
Myofibrillar myopathies (MFMs) are a group of hereditary neuromuscular disorders sharing common histological features, such as myofibrillar derangement, Z-disk disintegration, and the accumulation of degradation products into protein aggregates. They are caused by mutations in several genes that encode either structural proteins or molecular chaperones. Nevertheless, the mechanisms by which mutated genes result in protein aggregation are still unknown. To unveil the role of myotilin and αB-crystallin in the pathogenesis of MFM, we injected zebrafish fertilized eggs at the one-cell stage with expression plasmids harboring cDNA sequences of human wildtype or mutated MYOT (p.Ser95Ile) and human wildtype or mutated CRYAB (p.Gly154Ser). We evaluated the effects on fish survival, motor behavior, muscle structure and development. We found that transgenic zebrafish showed morphological defects that were more severe in those overexpressing mutant genes. which developed a myopathic phenotype consistent with that of human myofibrillar myopathy, including the formation of protein aggregates. Results indicate that pathogenic mutations in myotilin and αB-crystallin genes associated with MFM cause a structural and functional impairment of the skeletal muscle in zebrafish, thereby making this non-mammalian organism a powerful model to dissect disease pathogenesis and find possible druggable targets. Full article
(This article belongs to the Special Issue The Physiology of Striated Muscle Tissue 2.0)
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16 pages, 3367 KiB  
Article
Rbm20ΔRRM Mice, Expressing a Titin Isoform with Lower Stiffness, Are Protected from Mechanical Ventilation-Induced Diaphragm Weakness
by Marloes van den Berg, Eva L. Peters, Robbert J. van der Pijl, Shengyi Shen, Leo M. A. Heunks, Henk L. Granzier and Coen A. C. Ottenheijm
Int. J. Mol. Sci. 2022, 23(24), 15689; https://doi.org/10.3390/ijms232415689 - 10 Dec 2022
Cited by 2 | Viewed by 1797
Abstract
Diaphragm weakness frequently develops in mechanically ventilated critically ill patients and is associated with increased morbidity, including ventilator weaning failure, mortality, and health care costs. The mechanisms underlying diaphragm weakness are incompletely understood but may include the elastic properties of titin, a giant [...] Read more.
Diaphragm weakness frequently develops in mechanically ventilated critically ill patients and is associated with increased morbidity, including ventilator weaning failure, mortality, and health care costs. The mechanisms underlying diaphragm weakness are incompletely understood but may include the elastic properties of titin, a giant protein whose layout in the muscle’s sarcomeres makes it an ideal candidate to sense ventilation-induced diaphragm unloading, resulting in downstream signaling through titin-binding proteins. In the current study, we investigated whether modulating titin stiffness affects the development of diaphragm weakness during mechanical ventilation. To this end, we ventilated genetically engineered mice with reduced titin stiffness (Rbm20ΔRRM), and robust (TtnΔIAjxn) or severely (TtnΔ112–158) increased titin stiffness for 8 h, and assessed diaphragm contractility and protein expression of titin-binding proteins. Mechanical ventilation reduced the maximum active tension of the diaphragm in WT, TtnΔIAjxn and TtnΔ112–158 mice. However, in Rbm20ΔRRM mice maximum active tension was preserved after ventilation. Analyses of titin binding proteins suggest that muscle ankyrin repeat proteins (MARPs) 1 and 2 may play a role in the adaptation of the diaphragm to mechanical ventilation, and the preservation of diaphragm contractility in Rbm20ΔRRM mice. Thus, Rbm20ΔRRM mice, expressing titin isoforms with lower stiffness, are protected from mechanical ventilation-induced diaphragm weakness, suggesting that titin elasticity may modulate the diaphragm’s response to unloading during mechanical ventilation. Full article
(This article belongs to the Special Issue The Physiology of Striated Muscle Tissue 2.0)
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Review

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23 pages, 4275 KiB  
Review
Numerous Trigger-like Interactions of Kinases/Protein Phosphatases in Human Skeletal Muscles Can Underlie Transient Processes in Activation of Signaling Pathways during Exercise
by Alexander Yu. Vertyshev, Ilya R. Akberdin and Fedor A. Kolpakov
Int. J. Mol. Sci. 2023, 24(13), 11223; https://doi.org/10.3390/ijms241311223 - 07 Jul 2023
Viewed by 1187
Abstract
Optimizing physical training regimens to increase muscle aerobic capacity requires an understanding of the internal processes that occur during exercise that initiate subsequent adaptation. During exercise, muscle cells undergo a series of metabolic events that trigger downstream signaling pathways and induce the expression [...] Read more.
Optimizing physical training regimens to increase muscle aerobic capacity requires an understanding of the internal processes that occur during exercise that initiate subsequent adaptation. During exercise, muscle cells undergo a series of metabolic events that trigger downstream signaling pathways and induce the expression of many genes in working muscle fibers. There are a number of studies that show the dependence of changes in the activity of AMP-activated protein kinase (AMPK), one of the mediators of cellular signaling pathways, on the duration and intensity of single exercises. The activity of various AMPK isoforms can change in different directions, increasing for some isoforms and decreasing for others, depending on the intensity and duration of the load. This review summarizes research data on changes in the activity of AMPK, Ca2+/calmodulin-dependent protein kinase II (CaMKII), and other components of the signaling pathways in skeletal muscles during exercise. Based on these data, we hypothesize that the observed changes in AMPK activity may be largely related to metabolic and signaling transients rather than exercise intensity per se. Probably, the main events associated with these transients occur at the beginning of the exercise in a time window of about 1–10 min. We hypothesize that these transients may be partly due to putative trigger-like kinase/protein phosphatase interactions regulated by feedback loops. In addition, numerous dynamically changing factors, such as [Ca2+], metabolite concentration, and reactive oxygen and nitrogen species (RONS), can shift the switching thresholds and change the states of these triggers, thereby affecting the activity of kinases (in particular, AMPK and CaMKII) and phosphatases. The review considers the putative molecular mechanisms underlying trigger-like interactions. The proposed hypothesis allows for a reinterpretation of the experimental data available in the literature as well as the generation of ideas to optimize future training regimens. Full article
(This article belongs to the Special Issue The Physiology of Striated Muscle Tissue 2.0)
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16 pages, 2805 KiB  
Review
Insights into Cell-Specific Functions of Microtubules in Skeletal Muscle Development and Homeostasis
by Lathan Lucas and Thomas A. Cooper
Int. J. Mol. Sci. 2023, 24(3), 2903; https://doi.org/10.3390/ijms24032903 - 02 Feb 2023
Cited by 3 | Viewed by 2727
Abstract
The contractile cells of skeletal muscles, called myofibers, are elongated multinucleated syncytia formed and maintained by the fusion of proliferative myoblasts. Human myofibers can be hundreds of microns in diameter and millimeters in length. Myofibers are non-mitotic, obviating the need for microtubules in [...] Read more.
The contractile cells of skeletal muscles, called myofibers, are elongated multinucleated syncytia formed and maintained by the fusion of proliferative myoblasts. Human myofibers can be hundreds of microns in diameter and millimeters in length. Myofibers are non-mitotic, obviating the need for microtubules in cell division. However, microtubules have been adapted to the unique needs of these cells and are critical for myofiber development and function. Microtubules in mature myofibers are highly dynamic, and studies in several experimental systems have demonstrated the requirements for microtubules in the unique features of muscle biology including myoblast fusion, peripheral localization of nuclei, assembly of the sarcomere, transport and signaling. Microtubule-binding proteins have also been adapted to the needs of the skeletal muscle including the expression of skeletal muscle-specific protein isoforms generated by alternative splicing. Here, we will outline the different roles microtubules play in skeletal muscle cells, describe how microtubule abnormalities can lead to muscle disease and discuss the broader implications for microtubule function. Full article
(This article belongs to the Special Issue The Physiology of Striated Muscle Tissue 2.0)
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