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Skeletal Muscle Organelle Maintenance in Health and Disease: From Molecular Mechanisms to Practical Recommendations

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 March 2021) | Viewed by 29330

Special Issue Editor

Dr. Henri Bernardi

E-Mail Website
Guest Editor
DMEM, University of Montpellier, INRAE UMR866, 2 Place Pierre Viala, 34060 Montpellier, France
Interests: homeostasis of skeletal muscle; muscular atrophy and sarcopenia; proteasome and autophagy; exercise and countermeasures; protein synthesis and degradation

Special Issue Information

Dear Colleagues,

As skeletal muscle tissue maintenance is fundamental to whole-body homeostasis, disorders of its function or metabolism are linked to numerous diseases, such as metabolic syndrome, cancer- or sepsis- linked cachexia, and sarcopenia, as well as heart and renal failures. Among the different tissues, skeletal muscle has the peculiarity to continuously adapt itself to its environment and to display specific adaptive responses to several stimuli, such as contractile activity and nutritional status. Variations in muscle environmental factors induce transitory cellular stress leading to numerous adaptations, such as modifications in muscle size, fiber type composition, and contractile properties. Recent data on the ability of muscle cells to renew cellular proteins and organelles reveal essential molecular and cellular processes for organelle turnover, especially mitophagy and ribophagy. Dysregulation of organelle turnover in skeletal muscle is potentially implicated in many diseases and during aging. Factors such as AMPK, MTORC1, and FOXO play a central role in the control of organelles turnover and in the last few years other factors involved in muscle quality control and protein turnover, such as DGK, eIF3f, Apobec2, Parkin, Mul1, etc. have been pinpointed. In addition, recent studies have reported the effects of nutritional intake or physical exercise on the coordination of muscle organelle maintenance and renewal. An integrative view of all aspects of organelle turnover is paramount for a comprehensive understanding of adapted skeletal muscle response.

This Special Issue will highlight emerging research on the physiology and physiopathology associated with skeletal muscle organelle maintenance, with a special focus on nutritional and physical approaches. Original research articles, mini and full reviews, short communications, perspectives, and commentaries are welcome.

Dr. Henri Bernardi
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

  • Muscular homeostasis
  • Protein synthesis
  • Proteolysis
  • Muscle atrophy
  • Organelle turnover
  • Mitochondria
  • Exercise
  • Nutrition

Published Papers (5 papers)

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Research

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14 pages, 14050 KiB  
Article
Regulation of Glucose Metabolism by MuRF1 and Treatment of Myopathy in Diabetic Mice with Small Molecules Targeting MuRF1
by Siegfried Labeit, Stephanie Hirner, Julijus Bogomolovas, André Cruz, Moldir Myrzabekova, Anselmo Moriscot, Thomas Scott Bowen and Volker Adams
Int. J. Mol. Sci. 2021, 22(4), 2225; https://doi.org/10.3390/ijms22042225 - 23 Feb 2021
Cited by 12 | Viewed by 3302
Abstract
The muscle-specific ubiquitin ligase MuRF1 regulates muscle catabolism during chronic wasting states, although its roles in general metabolism are less-studied. Here, we metabolically profiled MuRF1-deficient knockout mice. We also included knockout mice for MuRF2 as its closely related gene homolog. MuRF1 and MuRF2-KO [...] Read more.
The muscle-specific ubiquitin ligase MuRF1 regulates muscle catabolism during chronic wasting states, although its roles in general metabolism are less-studied. Here, we metabolically profiled MuRF1-deficient knockout mice. We also included knockout mice for MuRF2 as its closely related gene homolog. MuRF1 and MuRF2-KO (knockout) mice have elevated serum glucose, elevated triglycerides, and reduced glucose tolerance. In addition, MuRF2-KO mice have a reduced tolerance to a fat-rich diet. Western blot and enzymatic studies on MuRF1-KO skeletal muscle showed perturbed FoxO-Akt signaling, elevated Akt-Ser-473 activation, and downregulated oxidative mitochondrial metabolism, indicating potential mechanisms for MuRF1,2-dependent glucose and fat metabolism regulation. Consistent with this, the adenoviral re-expression of MuRF1 in KO mice normalized Akt-Ser-473, serum glucose, and triglycerides. Finally, we tested the MuRF1/2 inhibitors MyoMed-205 and MyoMed-946 in a mouse model for type 2 diabetes mellitus (T2DM). After 28 days of treatment, T2DM mice developed progressive muscle weakness detected by wire hang tests, but this was attenuated by the MyoMed-205 treatment. While MyoMed-205 and MyoMed-946 had no significant effects on serum glucose, they did normalize the lymphocyte–granulocyte counts in diabetic sera as indicators of the immune response. Thus, small molecules directed to MuRF1 may be useful in attenuating skeletal muscle strength loss in T2DM conditions. Full article
(This article belongs to the Special Issue Skeletal Muscle Organelle Maintenance in Health and Disease: From Molecular Mechanisms to Practical Recommendations)
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21 pages, 4350 KiB  
Article
Plantar Mechanical Stimulation Maintains Slow Myosin Expression in Disused Rat Soleus Muscle via NO-Dependent Signaling
by Kristina A. Sharlo, Inna I. Paramonova, Irina D. Lvova, Ekaterina P. Mochalova, Vitaliy E. Kalashnikov, Natalia A. Vilchinskaya, Sergey A. Tyganov, Tatyana S. Konstantinova, Tatiana F. Shevchenko, Grigoriy R. Kalamkarov and Boris S. Shenkman
Int. J. Mol. Sci. 2021, 22(3), 1372; https://doi.org/10.3390/ijms22031372 - 29 Jan 2021
Cited by 18 | Viewed by 2075
Abstract
It was observed that gravitational unloading during space missions and simulated microgravity in ground-based studies leads to both transformation of slow-twitch muscle fibers into fast-twitch fibers and to the elimination of support afferentation, leading to the “switching-off” of postural muscle motor units electrical [...] Read more.
It was observed that gravitational unloading during space missions and simulated microgravity in ground-based studies leads to both transformation of slow-twitch muscle fibers into fast-twitch fibers and to the elimination of support afferentation, leading to the “switching-off” of postural muscle motor units electrical activity. In recent years, plantar mechanical stimulation (PMS) has been found to maintain the neuromuscular activity of the hindlimb muscles. Nitric oxide (NO) was shown to be one of the mediators of muscle fiber activity, which can also promote slow-type myosin expression. We hypothesized that applying PMS during rat hindlimb unloading would lead to NO production upregulation and prevention of the unloading-induced slow-to-fast fiber-type shift in rat soleus muscles. To test this hypothesis, Wistar rats were hindlimb suspended and subjected to daily PMS, and one group of PMS-subjected animals was also treated with nitric oxide synthase inhibitor (L-NAME). We discovered that PMS led to sustained NO level in soleus muscles of the suspended animals, and NOS inhibitor administration blocked this effect, as well as the positive effects of PMS on myosin I and IIa mRNA transcription and slow-to-fast fiber-type ratio during rat hindlimb unloading. The results of the study indicate that NOS activity is necessary for the PMS-mediated prevention of slow-to-fast fiber-type shift and myosin I and IIa mRNA transcription decreases during rat hindlimb unloading. Full article
(This article belongs to the Special Issue Skeletal Muscle Organelle Maintenance in Health and Disease: From Molecular Mechanisms to Practical Recommendations)
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Review

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16 pages, 1896 KiB  
Review
Cilia, Centrosomes and Skeletal Muscle
by Dominic C. H. Ng, Uda Y. Ho and Miranda D. Grounds
Int. J. Mol. Sci. 2021, 22(17), 9605; https://doi.org/10.3390/ijms22179605 - 04 Sep 2021
Cited by 8 | Viewed by 4319
Abstract
Primary cilia are non-motile, cell cycle-associated organelles that can be found on most vertebrate cell types. Comprised of microtubule bundles organised into an axoneme and anchored by a mature centriole or basal body, primary cilia are dynamic signalling platforms that are intimately involved [...] Read more.
Primary cilia are non-motile, cell cycle-associated organelles that can be found on most vertebrate cell types. Comprised of microtubule bundles organised into an axoneme and anchored by a mature centriole or basal body, primary cilia are dynamic signalling platforms that are intimately involved in cellular responses to their extracellular milieu. Defects in ciliogenesis or dysfunction in cilia signalling underlie a host of developmental disorders collectively referred to as ciliopathies, reinforcing important roles for cilia in human health. Whilst primary cilia have long been recognised to be present in striated muscle, their role in muscle is not well understood. However, recent studies indicate important contributions, particularly in skeletal muscle, that have to date remained underappreciated. Here, we explore recent revelations that the sensory and signalling functions of cilia on muscle progenitors regulate cell cycle progression, trigger differentiation and maintain a commitment to myogenesis. Cilia disassembly is initiated during myoblast fusion. However, the remnants of primary cilia persist in multi-nucleated myotubes, and we discuss their potential role in late-stage differentiation and myofiber formation. Reciprocal interactions between cilia and the extracellular matrix (ECM) microenvironment described for other tissues may also inform on parallel interactions in skeletal muscle. We also discuss emerging evidence that cilia on fibroblasts/fibro–adipogenic progenitors and myofibroblasts may influence cell fate in both a cell autonomous and non-autonomous manner with critical consequences for skeletal muscle ageing and repair in response to injury and disease. This review addresses the enigmatic but emerging role of primary cilia in satellite cells in myoblasts and myofibers during myogenesis, as well as the wider tissue microenvironment required for skeletal muscle formation and homeostasis. Full article
(This article belongs to the Special Issue Skeletal Muscle Organelle Maintenance in Health and Disease: From Molecular Mechanisms to Practical Recommendations)
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30 pages, 8446 KiB  
Review
Molecular Regulation of Skeletal Muscle Growth and Organelle Biosynthesis: Practical Recommendations for Exercise Training
by Robert Solsona, Laura Pavlin, Henri Bernardi and Anthony MJ Sanchez
Int. J. Mol. Sci. 2021, 22(5), 2741; https://doi.org/10.3390/ijms22052741 - 08 Mar 2021
Cited by 16 | Viewed by 9362
Abstract
The regulation of skeletal muscle mass and organelle homeostasis is dependent on the capacity of cells to produce proteins and to recycle cytosolic portions. In this investigation, the mechanisms involved in skeletal muscle mass regulation—especially those associated with proteosynthesis and with the production [...] Read more.
The regulation of skeletal muscle mass and organelle homeostasis is dependent on the capacity of cells to produce proteins and to recycle cytosolic portions. In this investigation, the mechanisms involved in skeletal muscle mass regulation—especially those associated with proteosynthesis and with the production of new organelles—are presented. Thus, the critical roles of mammalian/mechanistic target of rapamycin complex 1 (mTORC1) pathway and its regulators are reviewed. In addition, the importance of ribosome biogenesis, satellite cells involvement, myonuclear accretion, and some major epigenetic modifications related to protein synthesis are discussed. Furthermore, several studies conducted on the topic of exercise training have recognized the central role of both endurance and resistance exercise to reorganize sarcomeric proteins and to improve the capacity of cells to build efficient organelles. The molecular mechanisms underlying these adaptations to exercise training are presented throughout this review and practical recommendations for exercise prescription are provided. A better understanding of the aforementioned cellular pathways is essential for both healthy and sick people to avoid inefficient prescriptions and to improve muscle function with emergent strategies (e.g., hypoxic training). Finally, current limitations in the literature and further perspectives, notably on epigenetic mechanisms, are provided to encourage additional investigations on this topic. Full article
(This article belongs to the Special Issue Skeletal Muscle Organelle Maintenance in Health and Disease: From Molecular Mechanisms to Practical Recommendations)
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22 pages, 368 KiB  
Review
Skeletal Muscle Health and Cognitive Function: A Narrative Review
by Sophia X. Sui, Lana J. Williams, Kara L. Holloway-Kew, Natalie K. Hyde and Julie A. Pasco
Int. J. Mol. Sci. 2021, 22(1), 255; https://doi.org/10.3390/ijms22010255 - 29 Dec 2020
Cited by 90 | Viewed by 9397
Abstract
Sarcopenia is the loss of skeletal muscle mass and function with advancing age. It involves both complex genetic and modifiable risk factors, such as lack of exercise, malnutrition and reduced neurological drive. Cognitive decline refers to diminished or impaired mental and/or intellectual functioning. [...] Read more.
Sarcopenia is the loss of skeletal muscle mass and function with advancing age. It involves both complex genetic and modifiable risk factors, such as lack of exercise, malnutrition and reduced neurological drive. Cognitive decline refers to diminished or impaired mental and/or intellectual functioning. Contracting skeletal muscle is a major source of neurotrophic factors, including brain-derived neurotrophic factor, which regulate synapses in the brain. Furthermore, skeletal muscle activity has important immune and redox effects that modify brain function and reduce muscle catabolism. The identification of common risk factors and underlying mechanisms for sarcopenia and cognition may allow the development of targeted interventions that slow or reverse sarcopenia and also certain forms of cognitive decline. However, the links between cognition and skeletal muscle have not been elucidated fully. This review provides a critical appraisal of the literature on the relationship between skeletal muscle health and cognition. The literature suggests that sarcopenia and cognitive decline share pathophysiological pathways. Ageing plays a role in both skeletal muscle deterioration and cognitive decline. Furthermore, lifestyle risk factors, such as physical inactivity, poor diet and smoking, are common to both disorders, so their potential role in the muscle–brain relationship warrants investigation. Full article
(This article belongs to the Special Issue Skeletal Muscle Organelle Maintenance in Health and Disease: From Molecular Mechanisms to Practical Recommendations)
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