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Special Issue "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: 30 June 2021.

Special Issue Editors

Dr. Tatiana Kostrominova
E-Mail Website
Guest Editor
Department of Anatomy and Cell Biology, Indiana University School of Medicine Northwest, Gary, United States
Interests: Skeletal muscle; tendon; aging; denervation; obesity; myokines
Special Issues and Collections in MDPI journals
Dr. Susan V. Brooks
E-Mail Website
Guest Editor
University of Michigan, Ann Arbor, Ann Arbor, United States

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 papers will be 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.

Published Papers (2 papers)

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Research

Open AccessArticle
Insulin Resistance Is Not Sustained Following Denervation in Glycolytic Skeletal Muscle
Int. J. Mol. Sci. 2021, 22(9), 4913; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094913 - 06 May 2021
Viewed by 124
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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Open AccessArticle
Hyperbaric Oxygen Treatment Following Mid-Cervical Spinal Cord Injury Preserves Diaphragm Muscle Function
Int. J. Mol. Sci. 2020, 21(19), 7219; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21197219 - 30 Sep 2020
Cited by 1 | Viewed by 822
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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