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Skeletal Muscle Adaptations to Oxidative Stress
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Skeletal Muscle Adaptations to Oxidative Stress

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: 31 March 2025 | Viewed by 12106

Special Issue Editor

Dr. Guglielmo Duranti

E-Mail Website
Guest Editor
Unit of Biochemistry and Molecular Biology, Department of Movement, Human and Health Sciences, University of Rome FORO ITALICO, Piazza Lauro de Bosis 6, 00135 Rome, Italy
Interests: oxidative stress; skeletal muscle; physical activity; antioxidants; nutrition; aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Excessive stretching and intensive exercise which cause ruptures of myofibril filaments lead to skeletal muscle loss of function through the failure of the excitation–contraction coupling system. These events generate an inflammatory response and a higher reactive oxygen species (ROS) production. ROSs are continuously generated in the body and are usually promptly inactivated by the cellular antioxidant defenses. In skeletal muscle, low concentrations of ROS modulate cell signaling processes and are required for normal force production. Conversely, higher ROS concentrations can lead to DNA, lipid, protein, and carbohydrate modifications, causing cellular function impairment and a reduced force production and thereby contributing to muscle fatigue. For these reasons, the assessment of the impact of exercise at both the molecular and the biochemical levels, as well as its effect on cellular signaling pathways, constitute crucial points of interest for the development of training protocols that are compatible with the health of individuals. This Special Issue, entitled “Skeletal Muscle Adaptations to Oxidative Stress”, invites researchers to submit manuscripts. These may be either original research or reviews, with an emphasis on describing new biomarkers or novel exercise-regulated signaling pathways, as well as new techniques and research approaches involved in the interplay between oxidative stress, physical activity, nutritional strategies and skeletal muscle damage.The main focus of this SI is on human studies but work with animal models will also be considered.

Dr. Guglielmo Duranti
Guest Editor

Manuscript Submission Information

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Keywords

  • oxidative stress
  • exercise
  • physical activity
  • skeletal muscle
  • muscle damage
  • antioxidants
  • reactive oxygen species
  • redox balance
  • aging
  • nutrition

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Related Special Issue

Published Papers (5 papers)

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Research

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17 pages, 1134 KiB  
Article
Physical Activity and Epigenetic Aging in Breast Cancer Treatment
by Chantalle Moulton, Elisa Grazioli, José Santiago Ibáñez-Cabellos, Arianna Murri, Claudia Cerulli, Monica Silvestri, Daniela Caporossi, Federico V. Pallardó, José Luis García-Giménez, Stefano Magno, Cristina Rossi, Guglielmo Duranti, Salvador Mena-Molla, Attilio Parisi and Ivan Dimauro
Int. J. Mol. Sci. 2024, 25(16), 8596; https://doi.org/10.3390/ijms25168596 - 6 Aug 2024
Viewed by 1190
Abstract
Biological age, reflecting the cumulative damage in the body over a lifespan, is a dynamic measure more indicative of individual health than chronological age. Accelerated aging, when biological age surpasses chronological age, is implicated in poorer clinical outcomes, especially for breast cancer (BC) [...] Read more.
Biological age, reflecting the cumulative damage in the body over a lifespan, is a dynamic measure more indicative of individual health than chronological age. Accelerated aging, when biological age surpasses chronological age, is implicated in poorer clinical outcomes, especially for breast cancer (BC) survivors undergoing treatments. This preliminary study investigates the impact of a 16-week online supervised physical activity (PA) intervention on biological age in post-surgery female BC patients. Telomere length was measured using qPCR, and the ELOVL2-based epigenetic clock was assessed via DNA methylation pyrosequencing of the ELOVL2 promoter region. Telomere length remained unchanged, but the ELOVL2 epigenetic clock indicated a significant decrease in biological age in the PA group, suggesting the potential of PA interventions to reverse accelerated aging processes in BC survivors. The exercise group showed improved cardiovascular fitness, highlighting PA’s health impact. Finally, the reduction in biological age, as measured by the ELOVL2 epigenetic clock, was significantly associated with improvements in cardiovascular fitness and handgrip strength, supporting improved recovery. Epigenetic clocks can potentially assess health status and recovery progress in BC patients, identifying at-risk individuals in clinical practice. This study provides potential and valuable insights into how PA benefits BC survivors’ health, supporting the immediate benefits of a 16-week exercise intervention in mitigating accelerated aging. The findings could suggest a holistic approach to improving the health and recovery of post-surgery BC patients. Full article
(This article belongs to the Special Issue Skeletal Muscle Adaptations to Oxidative Stress)
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17 pages, 4534 KiB  
Article
Microdystrophin Gene Addition Significantly Improves Muscle Functionality and Diaphragm Muscle Histopathology in a Fibrotic Mouse Model of Duchenne Muscular Dystrophy
by Viktorija Cernisova, Ngoc Lu-Nguyen, Jessica Trundle, Shan Herath, Alberto Malerba and Linda Popplewell
Int. J. Mol. Sci. 2023, 24(9), 8174; https://doi.org/10.3390/ijms24098174 - 3 May 2023
Cited by 6 | Viewed by 3219
Abstract
Duchenne muscular dystrophy (DMD) is a rare neuromuscular disease affecting 1:5000 newborn males. No cure is currently available, but gene addition therapy, based on the adeno-associated viral (AAV) vector-mediated delivery of microdystrophin transgenes, is currently being tested in clinical trials. The muscles of [...] Read more.
Duchenne muscular dystrophy (DMD) is a rare neuromuscular disease affecting 1:5000 newborn males. No cure is currently available, but gene addition therapy, based on the adeno-associated viral (AAV) vector-mediated delivery of microdystrophin transgenes, is currently being tested in clinical trials. The muscles of DMD boys present significant fibrotic and adipogenic tissue deposition at the time the treatment starts. The presence of fibrosis not only worsens the disease pathology, but also diminishes the efficacy of gene therapy treatments. To gain an understanding of the efficacy of AAV-based microdystrophin gene addition in a relevant, fibrotic animal model of DMD, we conducted a systemic study in juvenile D2.mdx mice using the single intravenous administration of an AAV8 system expressing a sequence-optimized murine microdystrophin, named MD1 (AAV8-MD1). We mainly focused our study on the diaphragm, a respiratory muscle that is crucial for DMD pathology and that has never been analyzed after treatment with AAV-microdystrophin in this mouse model. We provide strong evidence here that the delivery of AAV8-MD1 provides significant improvement in body-wide muscle function. This is associated with the protection of the hindlimb muscle from contraction-induced damage and the prevention of fibrosis deposition in the diaphragm muscle. Our work corroborates the observation that the administration of gene therapy in DMD is beneficial in preventing muscle fibrosis. Full article
(This article belongs to the Special Issue Skeletal Muscle Adaptations to Oxidative Stress)
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21 pages, 7792 KiB  
Article
Effect of RONS-Induced Intracellular Redox Homeostasis in 6-NBDG/Glucose Uptake in C2C12 Myotubes and Single Isolated Skeletal Muscle Fibres
by Escarlata Fernández-Puente, Eva Martín-Prieto, Carlos Manuel Márquez and Jesús Palomero
Int. J. Mol. Sci. 2023, 24(9), 8082; https://doi.org/10.3390/ijms24098082 - 29 Apr 2023
Cited by 2 | Viewed by 1768
Abstract
The glucose uptake in skeletal muscle is essential to produce energy through ATP, which is needed by this organ to maintain vital functions. The impairment of glucose uptake compromises the metabolism and function of skeletal muscle and other organs and is a feature [...] Read more.
The glucose uptake in skeletal muscle is essential to produce energy through ATP, which is needed by this organ to maintain vital functions. The impairment of glucose uptake compromises the metabolism and function of skeletal muscle and other organs and is a feature of diabetes, obesity, and ageing. There is a need for research to uncover the mechanisms involved in the impairment of glucose uptake in skeletal muscle. In this study, we adapted, developed, optimised, and validated a methodology based on the fluorescence glucose analogue 6-NBDG, combined with a quantitative fluorescence microscopy image analysis, to determine the glucose uptake in two models of skeletal muscle cells: C2C12 myotubes and single fibres isolated from muscle. It was proposed that reactive oxygen and nitrogen species (RONS) and redox homeostasis play an important role in the modulation of intracellular redox signalling pathways associated with glucose uptake. In this study, we prove that the prooxidative intracellular redox environment under oxidative eustress produced by RONS such as hydrogen peroxide and nitric oxide improves glucose uptake in skeletal muscle cells. However, when oxidation is excessive, oxidative distress occurs, and cellular viability is compromised, although there might be an increase in the glucose uptake. Based on the results of this study, the determination of 6-NBDG/glucose uptake in myotubes and skeletal muscle cells is feasible, validated, and will contribute to improve future research. Full article
(This article belongs to the Special Issue Skeletal Muscle Adaptations to Oxidative Stress)
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Review

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26 pages, 1534 KiB  
Review
Advanced Cellular Models for Rare Disease Study: Exploring Neural, Muscle and Skeletal Organoids
by Cristina Bombieri, Andrea Corsi, Elisabetta Trabetti, Alessandra Ruggiero, Giulia Marchetto, Gaetano Vattemi, Maria Teresa Valenti, Donato Zipeto and Maria Grazia Romanelli
Int. J. Mol. Sci. 2024, 25(2), 1014; https://doi.org/10.3390/ijms25021014 - 13 Jan 2024
Cited by 5 | Viewed by 3217
Abstract
Organoids are self-organized, three-dimensional structures derived from stem cells that can mimic the structure and physiology of human organs. Patient-specific induced pluripotent stem cells (iPSCs) and 3D organoid model systems allow cells to be analyzed in a controlled environment to simulate the characteristics [...] Read more.
Organoids are self-organized, three-dimensional structures derived from stem cells that can mimic the structure and physiology of human organs. Patient-specific induced pluripotent stem cells (iPSCs) and 3D organoid model systems allow cells to be analyzed in a controlled environment to simulate the characteristics of a given disease by modeling the underlying pathophysiology. The recent development of 3D cell models has offered the scientific community an exceptionally valuable tool in the study of rare diseases, overcoming the limited availability of biological samples and the limitations of animal models. This review provides an overview of iPSC models and genetic engineering techniques used to develop organoids. In particular, some of the models applied to the study of rare neuronal, muscular and skeletal diseases are described. Furthermore, the limitations and potential of developing new therapeutic approaches are discussed. Full article
(This article belongs to the Special Issue Skeletal Muscle Adaptations to Oxidative Stress)
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19 pages, 6494 KiB  
Review
Effects of Hydrostatic-Pressure on Muscle Contraction: A Look Back on Some Experimental Findings
by K. W. Ranatunga and M. A. Geeves
Int. J. Mol. Sci. 2023, 24(5), 5031; https://doi.org/10.3390/ijms24055031 - 6 Mar 2023
Viewed by 2056
Abstract
Findings from experiments that used hydrostatic pressure changes to analyse the process of skeletal muscle contraction are re-examined. The force in resting muscle is insensitive to an increase in hydrostatic pressure from 0.1 MPa (atmospheric) to 10 MPa, as also found for force [...] Read more.
Findings from experiments that used hydrostatic pressure changes to analyse the process of skeletal muscle contraction are re-examined. The force in resting muscle is insensitive to an increase in hydrostatic pressure from 0.1 MPa (atmospheric) to 10 MPa, as also found for force in rubber-like elastic filaments. The force in rigour muscle rises with increased pressure, as shown experimentally for normal elastic fibres (e.g., glass, collagen, keratin, etc.). In submaximal active contractions, high pressure leads to tension potentiation. The force in maximally activated muscle decreases with increased pressure: the extent of this force decrease in maximal active muscle is sensitive to the concentration of products of ATP hydrolysis (Pi—inorganic phosphate and ADP—adenosine diphosphate) in the medium. When the increased hydrostatic pressure is rapidly decreased, the force recovered to the atmospheric level in all cases. Thus, the resting muscle force remained the same: the force in the rigour muscle decreased in one phase and that in active muscle increased in two phases. The rate of rise of active force on rapid pressure release increased with the concentration of Pi in the medium, indicating that it is coupled to the Pi release step in the ATPase-driven crossbridge cycle in muscle. Pressure experiments on intact muscle illustrate possible underlying mechanisms of tension potentiation and causes of muscle fatigue. Full article
(This article belongs to the Special Issue Skeletal Muscle Adaptations to Oxidative Stress)
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