Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.8
7.0
Journals
Antioxidants
Special Issues
Skeletal Muscle Redox Signaling and Metabolism
share announcement

Skeletal Muscle Redox Signaling and Metabolism

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 (15 March 2023) | Viewed by 4038

Special Issue Editor

Prof. Dr. Enrique Jaimovich

E-Mail Website
Guest Editor
Muscle Physiology Laboratory, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380000, Chile
Interests: skeletal muscle physiology; excitation–transcription coupling; gene expression; muscle metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

ROS play an important signaling role in skeletal muscle, closely associated with calcium signals that are not involved in muscle contraction. Several signaling pathways in striated muscle can be activated by an increase in reactive oxygen species (ROS) and reactive nitrogen species (RNS) production. Both the large magnitude of calcium signals involved in the contractile process and the deleterious processes induced by excess ROS/RNS production has made the study of the physiological role of ROS difficult and has restricted our in-depth research of these events for many years. Abnormal ROS/RNS production appears to be involved in several skeletal-muscle-related diseases, including muscle wasting, as in muscular dystrophies, aging-related sarcopenia and cancer cachexia. Metabolic diseases such as obesity are also related to abnormal ROS/RNS handling by muscle cells, leading to insulin resistance and T2D.

We invite you to submit your latest research findings or a review article to this Special Issue, which will collate current research in both skeletal muscle and exercise concerning ROS/RNS production, ROS/RNS regulation and ROS-/RNS-related deleterious processes and diseases. Collating this new knowledge of ROS/RNS homeostasis in skeletal muscle will provide important insights into the fine-tuning and physiological impact of important signaling within muscle cells.

Dr. Enrique Jaimovich
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. 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 2900 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

  • ROS sources
  • ROS metabolism
  • exercise-induced ROS/RNS
  • muscle antioxidants
  • abnormal ROS levels
  • ROS in muscle disease

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

27 pages, 15045 KiB  
Article
Melatonin Improves Skeletal Muscle Structure and Oxidative Phenotype by Regulating Mitochondrial Dynamics and Autophagy in Zücker Diabetic Fatty Rat
by Diego Salagre, Enrique Raya Álvarez, Cruz Miguel Cendan, Samira Aouichat and Ahmad Agil
Antioxidants 2023, 12(8), 1499; https://doi.org/10.3390/antiox12081499 - 27 Jul 2023
Cited by 2 | Viewed by 1841
Abstract
Obesity-induced skeletal muscle (SKM) inflexibility is closely linked to mitochondrial dysfunction. The present study aimed to evaluate the effects of melatonin on the red vastus lateralis (RVL) muscle in obese rat models at the molecular and morphological levels. Five-week-old male Zücker diabetic fatty [...] Read more.
Obesity-induced skeletal muscle (SKM) inflexibility is closely linked to mitochondrial dysfunction. The present study aimed to evaluate the effects of melatonin on the red vastus lateralis (RVL) muscle in obese rat models at the molecular and morphological levels. Five-week-old male Zücker diabetic fatty (ZDF) rats and their age-matched lean littermates (ZL) were orally treated either with melatonin (10 mg/kg body weight (BW)/24 h) (M–ZDF and M–ZL) or non-treated (control) (C–ZDF and C–ZL) for 12 weeks. Western blot analysis showed that mitochondrial fission, fusion, and autophagy were altered in the C-ZDF group, accompanied by reduced SIRT1 levels. Furthermore, C-ZDF rats exhibited depleted ATP production and nitro-oxidative stress, as indicated by increased nitrites levels and reduced SOD activity. Western blotting of MyH isoforms demonstrated a significant decrease in both slow and fast oxidative fiber-specific markers expression in the C-ZDF group, concomitant with an increase in the fast glycolytic fiber markers. At the tissue level, marked fiber atrophy, less oxidative fibers, and excessive lipid deposition were noted in the C-ZDF group. Interestingly, melatonin treatment partially restored mitochondrial fission/fusion imbalance in the RVL muscle by enhancing the expression of fission (Fis1 and DRP1) markers and decreasing that of fusion (OPA1 and Mfn2) markers. It was also found to restore autophagy, as indicated by increased p62 protein level and LC3BII/I ratio. In addition, melatonin treatment increased SIRT1 protein level, mitochondrial ATP production, and SOD activity and decreased nitrites production. These effects were associated with enhanced oxidative phenotype, as evidenced by amplified oxidative fiber-specific markers expression, histochemical reaction for NADH enzyme, and muscular lipid content. In this study, we showed that melatonin might have potential therapeutic implications for obesity-induced SKM metabolic inflexibility among patients with obesity and T2DM. Full article
(This article belongs to the Special Issue Skeletal Muscle Redox Signaling and Metabolism)
►▼ Show Figures

Graphical abstract

Review

Jump to: Research

15 pages, 1670 KiB  
Review
Energy (and Reactive Oxygen Species Generation) Saving Distribution of Mitochondria for the Activation of ATP Production in Skeletal Muscle
by Alejandra Espinosa, Mariana Casas and Enrique Jaimovich
Antioxidants 2023, 12(8), 1624; https://doi.org/10.3390/antiox12081624 - 17 Aug 2023
Cited by 2 | Viewed by 1722
Abstract
Exercise produces oxidants from a variety of intracellular sources, including NADPH oxidases (NOX) and mitochondria. Exercise-derived reactive oxygen species (ROS) are beneficial, and the amount and location of these ROS is important to avoid muscle damage associated with oxidative stress. We discuss here [...] Read more.
Exercise produces oxidants from a variety of intracellular sources, including NADPH oxidases (NOX) and mitochondria. Exercise-derived reactive oxygen species (ROS) are beneficial, and the amount and location of these ROS is important to avoid muscle damage associated with oxidative stress. We discuss here some of the evidence that involves ROS production associated with skeletal muscle contraction and the potential oxidative stress associated with muscle contraction. We also discuss the potential role of H2O2 produced after NOX activation in the regulation of glucose transport in skeletal muscle. Finally, we propose a model based on evidence for the role of different populations of mitochondria in skeletal muscle in the regulation of ATP production upon exercise. The subsarcolemmal population of mitochondria has the enzymatic and metabolic components to establish a high mitochondrial membrane potential when fissioned at rest but lacks the capacity to produce ATP. Calcium entry into the mitochondria will further increase the metabolic input. Upon exercise, subsarcolemmal mitochondria will fuse to intermyofibrillar mitochondria and will transfer the mitochondria membrane potential to them. These mitochondria are rich in ATP synthase and will subsequentially produce the ATP needed for muscle contraction in long-term exercise. These events will optimize energy use and minimize mitochondria ROS production. Full article
(This article belongs to the Special Issue Skeletal Muscle Redox Signaling and Metabolism)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop