Special Issue "Oxidative Stress and Skeletal Muscle Atrophy"

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 August 2021).

Special Issue Editors

Dr. Mitsuharu Okutsu
E-Mail Website
Guest Editor
Graduate School of Science Division of Biological Science, Nagoya City University, Nagoya, Aichi, Japan
Interests: muscle physiology and biology; oxidative stress; mitochondria biogenesis; angiogenesis; muscle fiber type switching; muscle contractile activity
Special Issues and Collections in MDPI journals
Dr. Vitor A. Lira
E-Mail Website
Guest Editor
Department of Health & Human Physiology, University of Iowa, Iowa City, IA 52242, USA
Interests: muscle biology; exercise physiology; substrate metabolism; proteostasis; gene regulation
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues, 

The journal Antioxidants is currently inviting submissions for a Special Issue entitled “Oxidative Stress and Skeletal Muscle Atrophy". 

Skeletal muscle atrophy contributes to morbidity and mortality in several conditions (e.g., aging, heart failure, cancer). It is known that oxidative stress can lead to skeletal muscle atrophy. However, our knowledge of the cellular and molecular mechanisms involved in oxidative-stress-induced atrophy, as well as a potential role for antioxidants in preserving muscle mass and strength in atrophying conditions, continues to evolve. 

In this Special Issue, we invite manuscript submissions that are focused on the physiology, cellular and molecular biology of oxidative stress and skeletal muscle atrophy. Studies in humans, animal models, or cultured cells are welcome. Major areas of importance include the impact of oxidative stress on (a) skeletal muscle mass and strength; (b) protein synthesis and degradation; (c) modifications to proteins, lipids or DNA; (d) mitochondrial function; (e) circulating or secreted mediators (e.g., cytokines, chemokines, and growth factors). Studies involving exercise, nutritional or antioxidant interventions are also of interest.

Dr. Mitsuharu Okutsu
Dr. Vitor A. Lira
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. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). 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
  • Oxidative stress
  • Atrophy
  • Aging
  • Sarcopenia
  • Heart failure
  • Cancer
  • Obesity
  • Diabetes
  • Disuse
  • Denervation
  • Antioxidants

Published Papers (1 paper)

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Research

Article
MG53 Preserves Neuromuscular Junction Integrity and Alleviates ALS Disease Progression
Antioxidants 2021, 10(10), 1522; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10101522 - 25 Sep 2021
Viewed by 308
Abstract
Respiratory failure from progressive respiratory muscle weakness is the most common cause of death in amyotrophic lateral sclerosis (ALS). Defects in neuromuscular junctions (NMJs) and progressive NMJ loss occur at early stages, thus stabilizing and preserving NMJs represents a potential therapeutic strategy to [...] Read more.
Respiratory failure from progressive respiratory muscle weakness is the most common cause of death in amyotrophic lateral sclerosis (ALS). Defects in neuromuscular junctions (NMJs) and progressive NMJ loss occur at early stages, thus stabilizing and preserving NMJs represents a potential therapeutic strategy to slow ALS disease progression. Here we demonstrate that NMJ damage is repaired by MG53, an intrinsic muscle protein involved in plasma membrane repair. Compromised diaphragm muscle membrane repair and NMJ integrity are early pathological events in ALS. Diaphragm muscles from ALS mouse models show increased susceptibility to injury and intracellular MG53 aggregation, which is also a hallmark of human muscle samples from ALS patients. We show that systemic administration of recombinant human MG53 protein in ALS mice protects against injury to diaphragm muscle, preserves NMJ integrity, and slows ALS disease progression. As MG53 is present in circulation in rodents and humans under physiological conditions, our findings provide proof-of-concept data supporting MG53 as a potentially safe and effective therapy to mitigate ALS progression. Full article
(This article belongs to the Special Issue Oxidative Stress and Skeletal Muscle Atrophy)
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