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Oxidative Stress and Skeletal Muscle Function

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: closed (31 December 2022) | Viewed by 17234

Special Issue Editor

Special Issue Information

Dear Colleagues,

Excessive stretching and intensive exercise causing rupture of myofibril filaments lead to skeletal muscle loss of function through the failure in the excitation–contraction coupling system. These events generate inflammatory response and an higher reactive oxygen species (ROS) production. ROS 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, while higher ROS concentrations can lead to DNA, lipid, protein, and carbohydrate modifications, which can cause cellular function impairment and a reduced force production 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 Oxidative Stress and Skeletal Muscle Function invites submissions of manuscripts, 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 is on human studies but work in animal models will also be considered.

Dr. Guglielmo Duranti
Guest Editor

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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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Published Papers (8 papers)

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Editorial

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6 pages, 591 KiB  
Editorial
Oxidative Stress and Skeletal Muscle Function
by Guglielmo Duranti
Int. J. Mol. Sci. 2023, 24(12), 10227; https://doi.org/10.3390/ijms241210227 - 16 Jun 2023
Viewed by 1051
Abstract
Skeletal muscle is continuously exposed during its activities to mechanical/oxidative damage [...] Full article
(This article belongs to the Special Issue Oxidative Stress and Skeletal Muscle Function)
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Research

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24 pages, 1432 KiB  
Article
The Influence of Single Whole-Body Cryostimulation on Cytokine Status and Oxidative Stress Biomarkers during Exhaustive Physical Effort: A Crossover Study
by Alicja Jurecka, Alina Woźniak, Celestyna Mila-Kierzenkowska, Beata Augustyńska, Łukasz Oleksy, Artur Stolarczyk and Artur Gądek
Int. J. Mol. Sci. 2023, 24(6), 5559; https://doi.org/10.3390/ijms24065559 - 14 Mar 2023
Cited by 3 | Viewed by 1501
Abstract
The purpose of the study was to assess the impact of single whole-body cryostimulation (WBC) preceding submaximal exercise on oxidative stress and inflammatory biomarkers in professional, male athletes. The subjects (n = 32, age 25.2 ± 37) were exposed to low temperatures [...] Read more.
The purpose of the study was to assess the impact of single whole-body cryostimulation (WBC) preceding submaximal exercise on oxidative stress and inflammatory biomarkers in professional, male athletes. The subjects (n = 32, age 25.2 ± 37) were exposed to low temperatures (−130 °C) in a cryochamber and then participated in 40 min of exercise (85% HRmax). Two weeks afterwards, the control exercise (without WBC) was performed. Blood samples were taken before the start of the study, immediately after the WBC procedure, after exercise preceded by WBC (WBC exercise) and after exercise without WBC. It has been shown that catalase activity after WBC exercise is lower in comparison with activity after control exercise. The interleukin 1β (IL-1-1β) level was higher after control exercise than after WBC exercise, after the WBC procedure and before the start of the study (p < 0.01). The WBC procedure interleukin 6 (IL-6) level was compared with the baseline level (p < 0.01). The level of Il-6 was higher both after WBC exercise and after control exercise compared with the level recorded after the WBC procedure (p < 0.05). Several significant correlations between the studied parameters were shown. In conclusion, the changes in the cytokine concentration in the athletes’ blood confirm that body exposition to extremely low temperatures before exercise could regulate the inflammatory reaction course and secretion of cytokines during exercise. A single session of WBC in the case of well-trained, male athletes does not significantly affect the level of oxidative stress indicators. Full article
(This article belongs to the Special Issue Oxidative Stress and Skeletal Muscle Function)
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15 pages, 2993 KiB  
Article
Phloroglucinol Inhibits Oxidative-Stress-Induced Cytotoxicity in C2C12 Murine Myoblasts through Nrf-2-Mediated Activation of HO-1
by Cheol Park, Hee-Jae Cha, Hyun Hwangbo, Seon Yeong Ji, Da Hye Kim, Min Yeong Kim, EunJin Bang, Su Hyun Hong, Sung Ok Kim, Soon-Jeong Jeong, Hyesook Lee, Sung-Kwon Moon, Jung-Hyun Shim, Gi-Young Kim, Suengmok Cho and Yung Hyun Choi
Int. J. Mol. Sci. 2023, 24(5), 4637; https://doi.org/10.3390/ijms24054637 - 27 Feb 2023
Cited by 3 | Viewed by 2032
Abstract
Phloroglucinol is a class of polyphenolic compounds containing aromatic phenyl rings and is known to have various pharmacological activities. Recently, we reported that this compound isolated from Ecklonia cava, a brown alga belonging to the family Laminariaceae, has potent antioxidant activity [...] Read more.
Phloroglucinol is a class of polyphenolic compounds containing aromatic phenyl rings and is known to have various pharmacological activities. Recently, we reported that this compound isolated from Ecklonia cava, a brown alga belonging to the family Laminariaceae, has potent antioxidant activity in human dermal keratinocytes. In this study, we evaluated whether phloroglucinol could protect against hydrogen peroxide (H2O2)-induced oxidative damage in murine-derived C2C12 myoblasts. Our results revealed that phloroglucinol suppressed H2O2-induced cytotoxicity and DNA damage while blocking the production of reactive oxygen species. We also found that phloroglucinol protected cells from the induction of apoptosis associated with mitochondrial impairment caused by H2O2 treatment. Furthermore, phloroglucinol enhanced the phosphorylation of nuclear factor-erythroid-2 related factor 2 (Nrf2) as well as the expression and activity of heme oxygenase-1 (HO-1). However, such anti-apoptotic and cytoprotective effects of phloroglucinol were greatly abolished by the HO-1 inhibitor, suggesting that phloroglucinol could increase the Nrf2-mediated activity of HO-1 to protect C2C12 myoblasts from oxidative stress. Taken together, our results indicate that phloroglucinol has a strong antioxidant activity as an Nrf2 activator and may have therapeutic benefits for oxidative-stress-mediated muscle disease. Full article
(This article belongs to the Special Issue Oxidative Stress and Skeletal Muscle Function)
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18 pages, 3812 KiB  
Article
Myomaker and Myomixer Characterization in Gilthead Sea Bream under Different Myogenesis Conditions
by Miquel Perelló-Amorós, Aitor Otero-Tarrazón, Violeta Jorge-Pedraza, Isabel García-Pérez, Albert Sánchez-Moya, Jean-Charles Gabillard, Fatemeh Moshayedi, Isabel Navarro, Encarnación Capilla, Jaume Fernández-Borràs, Josefina Blasco, Josep Chillarón, Daniel García de la serrana and Joaquim Gutiérrez
Int. J. Mol. Sci. 2022, 23(23), 14639; https://doi.org/10.3390/ijms232314639 - 24 Nov 2022
Cited by 5 | Viewed by 2051
Abstract
Skeletal muscle is formed by multinucleated myofibers originated by waves of hyperplasia and hypertrophy during myogenesis. Tissue damage triggers a regeneration process including new myogenesis and muscular remodeling. During myogenesis, the fusion of myoblasts is a key step that requires different genes’ expression, [...] Read more.
Skeletal muscle is formed by multinucleated myofibers originated by waves of hyperplasia and hypertrophy during myogenesis. Tissue damage triggers a regeneration process including new myogenesis and muscular remodeling. During myogenesis, the fusion of myoblasts is a key step that requires different genes’ expression, including the fusogens myomaker and myomixer. The present work aimed to characterize these proteins in gilthead sea bream and their possible role in in vitro myogenesis, at different fish ages and during muscle regeneration after induced tissue injury. Myomaker is a transmembrane protein highly conserved among vertebrates, whereas Myomixer is a micropeptide that is moderately conserved. myomaker expression is restricted to skeletal muscle, while the expression of myomixer is more ubiquitous. In primary myocytes culture, myomaker and myomixer expression peaked at day 6 and day 8, respectively. During regeneration, the expression of both fusogens and all the myogenic regulatory factors showed a peak after 16 days post-injury. Moreover, myomaker and myomixer were present at different ages, but in fingerlings there were significantly higher transcript levels than in juveniles or adult fish. Overall, Myomaker and Myomixer are valuable markers of muscle growth that together with other regulatory molecules can provide a deeper understanding of myogenesis regulation in fish. Full article
(This article belongs to the Special Issue Oxidative Stress and Skeletal Muscle Function)
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20 pages, 2847 KiB  
Article
The Impact of Spermidine on C2C12 Myoblasts Proliferation, Redox Status and Polyamines Metabolism under H2O2 Exposure
by Roberta Ceci, Guglielmo Duranti, Stefano Giuliani, Marianna Nicoletta Rossi, Ivan Dimauro, Stefania Sabatini, Paolo Mariottini and Manuela Cervelli
Int. J. Mol. Sci. 2022, 23(19), 10986; https://doi.org/10.3390/ijms231910986 - 20 Sep 2022
Cited by 6 | Viewed by 2187
Abstract
A central feature of the skeletal muscle is its ability to regenerate through the activation, by environmental signals, of satellite cells. Once activated, these cells proliferate as myoblasts, and defects in this process profoundly affect the subsequent process of regeneration. High levels of [...] Read more.
A central feature of the skeletal muscle is its ability to regenerate through the activation, by environmental signals, of satellite cells. Once activated, these cells proliferate as myoblasts, and defects in this process profoundly affect the subsequent process of regeneration. High levels of reactive oxygen species such as hydrogen peroxide (H2O2) with the consequent formation of oxidized macromolecules increase myoblasts’ cell death and strongly contribute to the loss of myoblast function. Recently, particular interest has turned towards the beneficial effects on muscle of the naturally occurring polyamine spermidine (Spd). In this work, we tested the hypothesis that Spd, upon oxidative challenge, would restore the compromised myoblasts’ viability and redox status. The effects of Spd in combination with aminoguanidine (Spd-AG), an inhibitor of bovine serum amine oxidase, on murine C2C12 myoblasts treated with a mild dose of H2O2 were evaluated by analyzing: (i) myoblast viability and recovery from wound scratch; (ii) redox status and (iii) polyamine (PAs) metabolism. The treatment of C2C12 myoblasts with Spd-AG increased cell number and accelerated scratch wound closure, while H2O2 exposure caused redox status imbalance and cell death. The combined treatment with Spd-AG showed an antioxidant effect on C2C12 myoblasts, partially restoring cellular total antioxidant capacity, reducing the oxidized glutathione (GSH/GSSG) ratio and increasing cell viability through a reduction in cell death. Moreover, Spd-AG administration counteracted the induction of polyamine catabolic genes and PA content decreased due to H2O2 challenges. In conclusion, our data suggest that Spd treatment has a protective role in skeletal muscle cells by restoring redox balance and promoting recovery from wound scratches, thus making myoblasts able to better cope with an oxidative insult. Full article
(This article belongs to the Special Issue Oxidative Stress and Skeletal Muscle Function)
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13 pages, 1934 KiB  
Article
Hydrogen Peroxide Stimulates Dihydrotestosterone Release in C2C12 Myotubes: A New Perspective for Exercise-Related Muscle Steroidogenesis?
by Cristina Antinozzi, Guglielmo Duranti, Roberta Ceci, Marco Lista, Stefania Sabatini, Daniela Caporossi, Luigi Di Luigi, Paolo Sgrò and Ivan Dimauro
Int. J. Mol. Sci. 2022, 23(12), 6566; https://doi.org/10.3390/ijms23126566 - 12 Jun 2022
Cited by 5 | Viewed by 2465
Abstract
Skeletal muscle is a tissue that has recently been recognized for its ability to produce androgens under physiological conditions. The steroidogenesis process is known to be negatively influenced by reactive oxygen species (ROS) in reproductive Leydig and ovary cells, while their effect on [...] Read more.
Skeletal muscle is a tissue that has recently been recognized for its ability to produce androgens under physiological conditions. The steroidogenesis process is known to be negatively influenced by reactive oxygen species (ROS) in reproductive Leydig and ovary cells, while their effect on muscle steroidogenesis is still an unexplored field. Muscle cells are continuously exposed to ROS, resulting from both their metabolic activity and the surrounding environment. Interestingly, the regulation of signaling pathways, induced by mild ROS levels, plays an important role in muscle fiber adaptation to exercise, in a process that also elicits a significant modulation in the hormonal response. The aim of the present study was to investigate whether ROS could influence steroidogenesis in skeletal muscle cells by evaluating the release of testosterone (T) and dihydrotestosterone (DHT), as well as the evaluation of the relative expression of the key steroidogenic enzymes 5α-reductase, 3β-hydroxysteroid dehydrogenase (HSD), 17β-HSD, and aromatase. C2C12 mouse myotubes were exposed to a non-cytotoxic concentration of hydrogen peroxide (H2O2), a condition intended to reproduce, in vitro, one of the main stimuli linked to the process of homeostasis and adaptation induced by exercise in skeletal muscle. Moreover, the influence of tadalafil (TAD), a phosphodiesterase 5 inhibitor (PDE5i) originally used to treat erectile dysfunction but often misused among athletes as a “performance-enhancing” drug, was evaluated in a single treatment or in combination with H2O2. Our data showed that a mild hydrogen peroxide exposure induced the release of DHT, but not T, and modulated the expression of the enzymes involved in steroidogenesis, while TAD treatment significantly reduced the H2O2-induced DHT release. This study adds a new piece of information about the adaptive skeletal muscle cell response to an oxidative environment, revealing that hydrogen peroxide plays an important role in activating muscle steroidogenesis. Full article
(This article belongs to the Special Issue Oxidative Stress and Skeletal Muscle Function)
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11 pages, 2260 KiB  
Article
Reduction of Superoxide Dismutase 1 Delays Regeneration of Cardiotoxin-Injured Skeletal Muscle in KK/Ta-Ins2Akita Mice with Progressive Diabetic Nephropathy
by Yuya Takahashi, Tatsunori Shimizu, Shunsuke Kato, Mitsuhiko Nara, Yumi Suganuma, Takehiro Sato, Tsukasa Morii, Yuichiro Yamada and Hiroki Fujita
Int. J. Mol. Sci. 2021, 22(11), 5491; https://doi.org/10.3390/ijms22115491 - 23 May 2021
Cited by 7 | Viewed by 2607
Abstract
Superoxide dismutase (SOD) is a major antioxidant enzyme for superoxide removal, and cytoplasmic SOD (SOD1) is expressed as a predominant isoform in all cells. We previously reported that renal SOD1 deficiency accelerates the progression of diabetic nephropathy (DN) via increasing renal oxidative stress. [...] Read more.
Superoxide dismutase (SOD) is a major antioxidant enzyme for superoxide removal, and cytoplasmic SOD (SOD1) is expressed as a predominant isoform in all cells. We previously reported that renal SOD1 deficiency accelerates the progression of diabetic nephropathy (DN) via increasing renal oxidative stress. To evaluate whether the degree of SOD1 expression determines regeneration capacity and sarcopenic phenotypes of skeletal muscles under incipient and advanced DN conditions, we investigated the alterations of SOD1 expression, oxidative stress marker, inflammation, fibrosis, and regeneration capacity in cardiotoxin (CTX)-injured tibialis anterior (TA) muscles of two Akita diabetic mouse models with different susceptibility to DN, DN-resistant C57BL/6-Ins2Akita and DN-prone KK/Ta-Ins2Akita mice. Here, we report that KK/Ta-Ins2Akita mice, but not C57BL/6-Ins2Akita mice, exhibit delayed muscle regeneration after CTX injection, as demonstrated by the finding indicating significantly smaller average cross-sectional areas of regenerating TA muscle myofibers relative to KK/Ta-wild-type mice. Furthermore, we observed markedly reduced SOD1 expression in CTX-injected TA muscles of KK/Ta-Ins2Akita mice, but not C57BL/6-Ins2Akita mice, along with increased inflammatory cell infiltration, prominent fibrosis and superoxide overproduction. Our study provides the first evidence that SOD1 reduction and the following superoxide overproduction delay skeletal muscle regeneration through induction of overt inflammation and fibrosis in a mouse model of progressive DN. Full article
(This article belongs to the Special Issue Oxidative Stress and Skeletal Muscle Function)
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Review

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12 pages, 1116 KiB  
Review
Pyroptosis and Insulin Resistance in Metabolic Organs
by Huiting Wei and Di Cui
Int. J. Mol. Sci. 2022, 23(19), 11638; https://doi.org/10.3390/ijms231911638 - 1 Oct 2022
Cited by 3 | Viewed by 2134
Abstract
Skeletal muscle serves as the optimal effective organ to balance glucose homeostasis, but insulin resistance (IR) in skeletal muscle breaks this balance by impeding glucose uptake and causes metabolic disorders. IR in skeletal muscle is caused by multiple factors, and it has been [...] Read more.
Skeletal muscle serves as the optimal effective organ to balance glucose homeostasis, but insulin resistance (IR) in skeletal muscle breaks this balance by impeding glucose uptake and causes metabolic disorders. IR in skeletal muscle is caused by multiple factors, and it has been reported that systemic low-grade inflammation is related to skeletal muscle IR, though its molecular mechanisms need to be ulteriorly studied. Pyroptosis is a novel inflammatory-mediated type of cell death. It has recently been reported that pyroptosis is associated with a decline in insulin sensitivity in skeletal muscle. The appropriate occurrence of pyroptosis positively eliminates pathogenic factors, whereas its excessive activation may aggravate inflammatory responses and expedite disease progression. The relationship between pyroptosis and IR in skeletal muscle and its underlined mechanism need to be further illustrated. The role of pyroptosis during the process of IR alleviation induced by non-drug interventions, such as exercise, also needs to be clarified. In this paper, we review and describe the molecular mechanisms of pyroptosis and further comb the roles of its relevant key factors in skeletal muscle IR, aiming to propose a novel theoretical basis for the relationship between pyroptosis and muscle IR and provide new research targets for the improvement of IR-related diseases. Full article
(This article belongs to the Special Issue Oxidative Stress and Skeletal Muscle Function)
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