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Skeletal Muscle Denervation
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Skeletal Muscle Denervation

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

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 39174

Special Issue Editors

Dr. Tatiana Kostrominova

E-Mail Website
Guest Editor
Department of Anatomy and Cell Biology, Indiana University School of Medicine-Northwest, 3400 Broadway St., Gary, IN 46408-1197, USA
Interests: skeletal muscle; tendon; aging; muscle denervation; muscle unloading; obesity; myokines
Special Issues, Collections and Topics in MDPI journals
Dr. Susan V. Brooks

E-Mail Website
Guest Editor
University of Michigan, Ann Arbor, Ann Arbor, MI, USA

Special Issue Information

Skeletal muscle is a second largest organ of the human body. In addition to its essential role for locomotion, maintaining posture, respiration (diaphragm), and phonation (laryngeal muscles), skeletal muscle plays a critical role in whole-body metabolism. Skeletal muscle is a major organ responsible for insulin-stimulated glucose utilization in humans. Myokine secreted by skeletal muscle can affect the metabolism of distant organs, including the liver and adipose tissue.

Normal skeletal muscle development, structural organization, and function require innervation. Loss of muscle innervation during development results in a defective musculoskeletal unit (muscle–tendon–bone) structure. Loss of muscle innervation in a mature muscle leads to the loss of contractile proteins and to muscle atrophy.

Skeletal muscle denervation has been the focus of many studies that have uncovered multiple complex and often intertwined mechanisms. Nevertheless, many aspects of muscle denervation and especially the approaches to the prevention and treatment of denervation-induced muscle atrophy are still not completely understood. A better understanding of the mechanisms regulating skeletal muscle denervation will enable the prevention and treatment of the denervation-induced muscle dysfunction. In this Special Issue titled “Skeletal Muscle Denervation”, we would like to highlight the latest advances in this research topic.

We invite authors to submit original research and review articles revealing the molecular mechanisms of skeletal muscle denervation, including, but not limited to, the following topics:

  • Denervation-induced developmental skeletal muscle abnormalities;
  • Denervation-induced skeletal muscle atrophy;
  • Aging-related skeletal muscle denervation;
  • Diseases associated with skeletal muscle denervation;
  • Signaling involved in skeletal muscle denervation;
  • Denervation-induced changes in gene expression in skeletal muscle;
  • Oxidative and endoplasmic reticulum stress activated in response to skeletal muscle denervation;
  • Denervation-related changes in myokine expression/secretion in skeletal muscle.

Dr. Tatiana Kostrominova
Dr. Susan V. Brooks
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.

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Published Papers (7 papers)

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Editorial

Jump to: Research, Review

4 pages, 637 KiB  
Editorial
Skeletal Muscle Denervation: Past, Present and Future
by Tatiana Y. Kostrominova
Int. J. Mol. Sci. 2022, 23(14), 7489; https://doi.org/10.3390/ijms23147489 - 6 Jul 2022
Cited by 16 | Viewed by 5957
Abstract
This Special Issue presents some of the most recent studies on the skeletal muscle denervation [...] Full article
(This article belongs to the Special Issue Skeletal Muscle Denervation)
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Research

Jump to: Editorial, Review

19 pages, 3235 KiB  
Article
Deletion of Neuronal CuZnSOD Accelerates Age-Associated Muscle Mitochondria and Calcium Handling Dysfunction That Is Independent of Denervation and Precedes Sarcopenia
by Yu Su, Dennis R. Claflin, Meixiang Huang, Carol S. Davis, Peter C. D. Macpherson, Arlan Richardson, Holly Van Remmen and Susan V. Brooks
Int. J. Mol. Sci. 2021, 22(19), 10735; https://doi.org/10.3390/ijms221910735 - 4 Oct 2021
Cited by 15 | Viewed by 3190
Abstract
Skeletal muscle suffers atrophy and weakness with aging. Denervation, oxidative stress, and mitochondrial dysfunction are all proposed as contributors to age-associated muscle loss, but connections between these factors have not been established. We examined contractility, mitochondrial function, and intracellular calcium transients (ICTs) in [...] Read more.
Skeletal muscle suffers atrophy and weakness with aging. Denervation, oxidative stress, and mitochondrial dysfunction are all proposed as contributors to age-associated muscle loss, but connections between these factors have not been established. We examined contractility, mitochondrial function, and intracellular calcium transients (ICTs) in muscles of mice throughout the life span to define their sequential relationships. We performed these same measures and analyzed neuromuscular junction (NMJ) morphology in mice with postnatal deletion of neuronal Sod1 (i-mn-Sod1-/- mice), previously shown to display accelerated age-associated muscle loss and exacerbation of denervation in old age, to test relationships between neuronal redox homeostasis, NMJ degeneration and mitochondrial function. In control mice, the amount and rate of the decrease in mitochondrial NADH during contraction was greater in middle than young age although force was not reduced, suggesting decreased efficiency of NADH utilization prior to the onset of weakness. Declines in both the peak of the ICT and force were observed in old age. Muscles of i-mn-Sod1-/- mice showed degeneration of mitochondrial and calcium handling functions in middle-age and a decline in force generation to a level not different from the old control mice, with maintenance of NMJ morphology. Together, the findings support the conclusion that muscle mitochondrial function decreases during aging and in response to altered neuronal redox status prior to NMJ deterioration or loss of mass and force suggesting mitochondrial defects contribute to sarcopenia independent of denervation. Full article
(This article belongs to the Special Issue Skeletal Muscle Denervation)
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13 pages, 2081 KiB  
Article
Insulin Resistance Is Not Sustained Following Denervation in Glycolytic Skeletal Muscle
by Shawna L. McMillin, Erin C. Stanley, Luke A. Weyrauch, Jeffrey J. Brault, Barbara B. Kahn and Carol A. Witczak
Int. J. Mol. Sci. 2021, 22(9), 4913; https://doi.org/10.3390/ijms22094913 - 6 May 2021
Cited by 5 | Viewed by 3038
Abstract
Denervation rapidly induces insulin resistance (i.e., impairments in insulin-stimulated glucose uptake and signaling proteins) in skeletal muscle. Surprisingly, whether this metabolic derangement is long-lasting is presently not clear. The main goal of this study was to determine if insulin resistance is sustained in [...] Read more.
Denervation rapidly induces insulin resistance (i.e., impairments in insulin-stimulated glucose uptake and signaling proteins) in skeletal muscle. Surprisingly, whether this metabolic derangement is long-lasting is presently not clear. The main goal of this study was to determine if insulin resistance is sustained in both oxidative soleus and glycolytic extensor digitorum longus (EDL) muscles following long-term (28 days) denervation. Mouse hindlimb muscles were denervated via unilateral sciatic nerve resection. Both soleus and EDL muscles atrophied ~40%. Strikingly, while denervation impaired submaximal insulin-stimulated [3H]-2-deoxyglucose uptake ~30% in the soleus, it enhanced submaximal (~120%) and maximal (~160%) insulin-stimulated glucose uptake in the EDL. To assess possible mechanism(s), immunoblots were performed. Denervation did not consistently alter insulin signaling (e.g., p-Akt (Thr308):Akt; p-TBC1D1 [phospho-Akt substrate (PAS)]:TBC1D1; or p-TBC1D4 (PAS):TBC1D4) in either muscle. However, denervation decreased glucose transporter 4 (GLUT4) levels ~65% in the soleus but increased them ~90% in the EDL. To assess the contribution of GLUT4 to the enhanced EDL muscle glucose uptake, muscle-specific GLUT4 knockout mice were examined. Loss of GLUT4 prevented the denervation-induced increase in insulin-stimulated glucose uptake. In conclusion, the denervation results sustained insulin resistance in the soleus but enhanced insulin sensitivity in the EDL due to increased GLUT4 protein levels. Full article
(This article belongs to the Special Issue Skeletal Muscle Denervation)
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12 pages, 1862 KiB  
Article
Hyperbaric Oxygen Treatment Following Mid-Cervical Spinal Cord Injury Preserves Diaphragm Muscle Function
by Ashley J. Smuder, Sara M. Turner, Cassandra M. Schuster, Aaron B. Morton, J. Matthew Hinkley and David D. Fuller
Int. J. Mol. Sci. 2020, 21(19), 7219; https://doi.org/10.3390/ijms21197219 - 30 Sep 2020
Cited by 17 | Viewed by 4101
Abstract
Oxidative damage to the diaphragm as a result of cervical spinal cord injury (SCI) promotes muscle atrophy and weakness. Respiratory insufficiency is the leading cause of morbidity and mortality in cervical spinal cord injury (SCI) patients, emphasizing the need for strategies to maintain [...] Read more.
Oxidative damage to the diaphragm as a result of cervical spinal cord injury (SCI) promotes muscle atrophy and weakness. Respiratory insufficiency is the leading cause of morbidity and mortality in cervical spinal cord injury (SCI) patients, emphasizing the need for strategies to maintain diaphragm function. Hyperbaric oxygen (HBO) increases the amount of oxygen dissolved into the blood, elevating the delivery of oxygen to skeletal muscle and reactive oxygen species (ROS) generation. It is proposed that enhanced ROS production due to HBO treatment stimulates adaptations to diaphragm oxidative capacity, resulting in overall reductions in oxidative stress and inflammation. Therefore, we tested the hypothesis that exposure to HBO therapy acutely following SCI would reduce oxidative damage to the diaphragm muscle, preserving muscle fiber size and contractility. Our results demonstrated that lateral contusion injury at C3/4 results in a significant reduction in diaphragm muscle-specific force production and fiber cross-sectional area, which was associated with augmented mitochondrial hydrogen peroxide emission and a reduced mitochondrial respiratory control ratio. In contrast, rats that underwent SCI followed by HBO exposure consisting of 1 h of 100% oxygen at 3 atmospheres absolute (ATA) delivered for 10 consecutive days demonstrated an improvement in diaphragm-specific force production, and an attenuation of fiber atrophy, mitochondrial dysfunction and ROS production. These beneficial adaptations in the diaphragm were related to HBO-induced increases in antioxidant capacity and a reduction in atrogene expression. These findings suggest that HBO therapy may be an effective adjunctive therapy to promote respiratory health following cervical SCI. Full article
(This article belongs to the Special Issue Skeletal Muscle Denervation)
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Review

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8 pages, 447 KiB  
Review
Transforming Growth Factor-Beta in Skeletal Muscle Wasting
by Gordon L. Klein
Int. J. Mol. Sci. 2022, 23(3), 1167; https://doi.org/10.3390/ijms23031167 - 21 Jan 2022
Cited by 15 | Viewed by 2729
Abstract
Transforming growth factor-beta (TGF-β) is part of a family of molecules that is present in many body tissues and performs many different functions. Evidence has been obtained from mice and human cancer patients with bony metastases and non-metastatic disease, as well as pediatric [...] Read more.
Transforming growth factor-beta (TGF-β) is part of a family of molecules that is present in many body tissues and performs many different functions. Evidence has been obtained from mice and human cancer patients with bony metastases and non-metastatic disease, as well as pediatric burn patients, that inflammation leads to bone resorption and release of TGF-β from the bone matrix with paracrine effects on muscle protein balance, possibly mediated by the generation of reactive oxygen species. Whether immobilization, which confounds the etiology of bone resorption in burn injury, also leads to the release of TGF-β from bone contributing to muscle wasting in other conditions is unclear. The use of anti-resorptive therapy in both metastatic cancer patients and pediatric burn patients has been successful in the prevention of muscle wasting, thereby creating an additional therapeutic niche for this class of drugs. The liberation of TGF-β may be one way in which bone helps to control muscle mass, but further investigation will be necessary to assess whether the rate of bone resorption is the determining factor for the release of TGF-β. Moreover, whether different resorptive conditions, such as immobilization and hyperparathyroidism, also involve TGF-β release in the pathogenesis of muscle wasting needs to be investigated. Full article
(This article belongs to the Special Issue Skeletal Muscle Denervation)
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20 pages, 1476 KiB  
Review
Natural Compounds Attenuate Denervation-Induced Skeletal Muscle Atrophy
by Tomohiko Shirakawa, Aki Miyawaki, Tatsuo Kawamoto and Shoichiro Kokabu
Int. J. Mol. Sci. 2021, 22(15), 8310; https://doi.org/10.3390/ijms22158310 - 2 Aug 2021
Cited by 8 | Viewed by 6707
Abstract
The weight of skeletal muscle accounts for approximately 40% of the whole weight in a healthy individual, and the normal metabolism and motor function of the muscle are indispensable for healthy life. In addition, the skeletal muscle of the maxillofacial region plays an [...] Read more.
The weight of skeletal muscle accounts for approximately 40% of the whole weight in a healthy individual, and the normal metabolism and motor function of the muscle are indispensable for healthy life. In addition, the skeletal muscle of the maxillofacial region plays an important role not only in eating and swallowing, but also in communication, such as facial expressions and conversations. In recent years, skeletal muscle atrophy has received worldwide attention as a serious health problem. However, the mechanism of skeletal muscle atrophy that has been clarified at present is insufficient, and a therapeutic method against skeletal muscle atrophy has not been established. This review provides views on the importance of skeletal muscle in the maxillofacial region and explains the differences between skeletal muscles in the maxillofacial region and other regions. We summarize the findings to change in gene expression in muscle remodeling and emphasize the advantages and disadvantages of denervation-induced skeletal muscle atrophy model. Finally, we discuss the newly discovered beneficial effects of natural compounds on skeletal muscle atrophy. Full article
(This article belongs to the Special Issue Skeletal Muscle Denervation)
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17 pages, 1368 KiB  
Review
The Neuromuscular Junction: Roles in Aging and Neuromuscular Disease
by Shama R. Iyer, Sameer B. Shah and Richard M. Lovering
Int. J. Mol. Sci. 2021, 22(15), 8058; https://doi.org/10.3390/ijms22158058 - 28 Jul 2021
Cited by 48 | Viewed by 12127
Abstract
The neuromuscular junction (NMJ) is a specialized synapse that bridges the motor neuron and the skeletal muscle fiber and is crucial for conversion of electrical impulses originating in the motor neuron to action potentials in the muscle fiber. The consideration of contributing factors [...] Read more.
The neuromuscular junction (NMJ) is a specialized synapse that bridges the motor neuron and the skeletal muscle fiber and is crucial for conversion of electrical impulses originating in the motor neuron to action potentials in the muscle fiber. The consideration of contributing factors to skeletal muscle injury, muscular dystrophy and sarcopenia cannot be restricted only to processes intrinsic to the muscle, as data show that these conditions incur denervation-like findings, such as fragmented NMJ morphology and corresponding functional changes in neuromuscular transmission. Primary defects in the NMJ also influence functional loss in motor neuron disease, congenital myasthenic syndromes and myasthenia gravis, resulting in skeletal muscle weakness and heightened fatigue. Such findings underscore the role that the NMJ plays in neuromuscular performance. Regardless of cause or effect, functional denervation is now an accepted consequence of sarcopenia and muscle disease. In this short review, we provide an overview of the pathologic etiology, symptoms, and therapeutic strategies related to the NMJ. In particular, we examine the role of the NMJ as a disease modifier and a potential therapeutic target in neuromuscular injury and disease. Full article
(This article belongs to the Special Issue Skeletal Muscle Denervation)
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