Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
10.6
6.0
Journals
Antioxidants
Special Issues
Oxidative Stress in Skeletal Muscle
share announcement

Oxidative Stress in Skeletal Muscle

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 May 2021) | Viewed by 32285

Special Issue Editor

Prof. Dr. Stefania Fulle

E-Mail Website
Guest Editor
Department of Neuroscience, Imaging and Clinical Sciences, University ”G. d’Annunzio” Chieti-Pescara, 66100 Chieti, Italy
Interests: oxidative stress and antioxidant enzymes; cellular signalling; growth factors; muscular trophism; muscle stem cells; regenerative aspects of space flight; sarcopenia
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The skeletal muscle is a tissue in which the generation of free radicals, including reactive oxygen species (ROS), is more pronounced. Generation of ROS represents one of the most prominent events during contractile activity, suggesting that it could affect muscle function and health. The production of ROS is often associated with the term oxidative stress, used to define a "pathological" condition. Despite, however, the ROS formation having for a long time been believed harmful, evidence is accumulating for an important role of ROS in cell signaling. It has been proposed that several factors, including ROS, are able to regulate skeletal muscle gene expression, modulating the transcriptional profile of many genes. Furthermore, some evidence is accumulating on the role of ROS also in the modulation of miRNAs involved in muscle remodeling. The cumulative oxidative damage appears to have a strong correlation with senescence and, particularly, with sarcopenia, the physiological condition of elderly skeletal muscle. Normally, there is a balance between free radicals’ production and the intrinsic repair system of the cell, which if disturbed can lead to an increase in oxidative damage to the cell. Indeed, the cells respond to oxidative stress episodes in order to prevent further tissue damage, and that failure to respond in this way is a feature of the aging process.

How do ROS act as physiological signaling molecules, though? When does oxidative stress become a harmful factor?

In this Special Issue, we invite researchers to provide original research articles and review articles regarding results in the field of oxidative stress that are negative and/or positive for skeletal muscle, with particular attention to the role of ROS, both at cellular and molecular level, at the basis of functional and homeostatic mechanisms.

As Guest Editor, I invite you to contribute to this Special Issue on “Oxidative Stress in Skeletal Muscle”. Original research reports and reviews will be published online in Antioxidants.

Prof. Dr. Stefania Fulle
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

  • Oxidative stress
  • Muscle Aging
  • Skeletal muscle homeostasis
  • Antioxidant systems
  • ROS in cell signaling

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (9 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:

Editorial

Jump to: Research, Review

5 pages, 1521 KiB  
Editorial
Oxidative Stress in Skeletal Muscle
by Giorgio Fanò-Illic and Stefania Fulle
Antioxidants 2022, 11(7), 1299; https://doi.org/10.3390/antiox11071299 - 29 Jun 2022
Cited by 1 | Viewed by 1389
Abstract
The accumulation of ROS, mainly due to increased mitochondrial production and/or decreased scavenger systems, is often associated with the term oxidative stress, used to define a condition judged to be problematic for muscle cells [...] Full article
(This article belongs to the Special Issue Oxidative Stress in Skeletal Muscle)
►▼ Show Figures

Figure 1

Research

Jump to: Editorial, Review

11 pages, 2110 KiB  
Article
Curcuma longa L. Water Extract Improves Dexamethasone-Induced Sarcopenia by Modulating the Muscle-Related Gene and Oxidative Stress in Mice
by Shintae Kim, Kyungmi Kim, Jeongjin Park and Woojin Jun
Antioxidants 2021, 10(7), 1000; https://doi.org/10.3390/antiox10071000 - 23 Jun 2021
Cited by 22 | Viewed by 4798
Abstract
Dexamethasone (DEX) promotes proteolysis, which causes muscle atrophy. Muscle atrophy is connected to sarcopenia. We evaluated the effect of Curcuma longa L. water extract (CLW) on DEX-induced muscle atrophy. ICR mice were divided into three groups (eight mice per group) to investigate the [...] Read more.
Dexamethasone (DEX) promotes proteolysis, which causes muscle atrophy. Muscle atrophy is connected to sarcopenia. We evaluated the effect of Curcuma longa L. water extract (CLW) on DEX-induced muscle atrophy. ICR mice were divided into three groups (eight mice per group) to investigate the capability of CLW in inhibiting muscle atrophy. The control group (Ex-CON) was administered distilled water (DW) by gavage and subjected to exercise; the muscle atrophy group (Ex-DEX) was administered DW by gavage, an injection of DEX (1 mg/kg body weight/day) intraperitoneally (IP), and subjected to exercise; and the treatment group (Ex-CLW) was administered CLW (1 g/kg body weight/day) by gavage, DEX IP injection, and subjected to exercise. Following the injection of DEX, the expression levels of myostatin, MuRF-1, and Atrogin-1 were increased. However, these expression levels were decreased in the Ex-CLW group, thereby leading to the conclusion that CLW inhibits muscle atrophy. ROS (that was overproduced by DEX) decreased antioxidant enzyme activity and increased malondialdehyde (MDA) levels, which led to muscle atrophy. When CLW was ingested, the antioxidant enzyme activities increased while the MDA levels decreased. These findings suggest that CLW could serve as a natural product for the prevention of muscle atrophy by modulating muscle atrophy-related genes and increasing antioxidant potential. Full article
(This article belongs to the Special Issue Oxidative Stress in Skeletal Muscle)
►▼ Show Figures

Figure 1

14 pages, 2739 KiB  
Article
Skeletal Lipocalin-2 Is Associated with Iron-Related Oxidative Stress in ob/ob Mice with Sarcopenia
by Eun Bee Choi, Jae Hun Jeong, Hye Min Jang, Yu Jeong Ahn, Kyu Hyeon Kim, Hyeong Seok An, Jong Youl Lee, Eun Ae Jeong, Jaewoong Lee, Hyun Joo Shin, Kyung Eun Kim and Gu Seob Roh
Antioxidants 2021, 10(5), 758; https://doi.org/10.3390/antiox10050758 - 11 May 2021
Cited by 15 | Viewed by 3637
Abstract
Obesity and insulin resistance accelerate aging-related sarcopenia, which is associated with iron load and oxidative stress. Lipocalin-2 (LCN2) is an iron-binding protein that has been associated with skeletal muscle regeneration, but details regarding its role in obese sarcopenia remain unclear. Here, we report [...] Read more.
Obesity and insulin resistance accelerate aging-related sarcopenia, which is associated with iron load and oxidative stress. Lipocalin-2 (LCN2) is an iron-binding protein that has been associated with skeletal muscle regeneration, but details regarding its role in obese sarcopenia remain unclear. Here, we report that elevated LCN2 levels in skeletal muscle are linked to muscle atrophy-related inflammation and oxidative stress in leptin-deficient ob/ob mice. RNA sequencing analyses indicated the LCN2 gene expression is enhanced in skeletal muscle of ob/ob mice with sarcopenia. In addition to muscular iron accumulation in ob/ob mice, expressions of iron homeostasis-related divalent metal transporter 1, ferritin, and hepcidin proteins were increased in ob/ob mice compared to lean littermates, whereas expressions of transferrin receptor and ferroportin were reduced. Collectively, these findings demonstrate that LCN2 functions as a potent proinflammatory factor in skeletal muscle in response to obesity-related sarcopenia and is thus a therapeutic candidate target for sarcopenia treatment. Full article
(This article belongs to the Special Issue Oxidative Stress in Skeletal Muscle)
►▼ Show Figures

Figure 1

16 pages, 4095 KiB  
Article
To Synthesize Hydroxyapatite by Modified Low Temperature Method Loaded with Bletilla striata Polysaccharide as Antioxidant for the Prevention of Sarcopenia by Intramuscular Administration
by Ya-Jyun Liang, Jia-Yu Hong, I-Hsuan Yang, Xin-Ran Zhou, Yi-Wen Lin, Tzu-Chieh Lin, Chun-Han Hou and Feng-Huei Lin
Antioxidants 2021, 10(3), 488; https://doi.org/10.3390/antiox10030488 - 20 Mar 2021
Cited by 14 | Viewed by 3213
Abstract
Oxidative stress has been suggested as an important factor in the progress of sarcopenia. The current treatments for sarcopenia have the disadvantages of insufficient effect or daily administration. Therefore, an alternative for effective, safety and long-term treatment may be a solution for unmet [...] Read more.
Oxidative stress has been suggested as an important factor in the progress of sarcopenia. The current treatments for sarcopenia have the disadvantages of insufficient effect or daily administration. Therefore, an alternative for effective, safety and long-term treatment may be a solution for unmet needs. Bletilla striata polysaccharide has been reported to have anti­oxidative and anti-inflammatory properties. In this study, we used Bletilla striata polysaccharide (BSP) combined with hydroxyapatite, a carrier. We hypothesized that the resulting combination (BSP-HAP) is a good formula for the controlled release of BSP via intramuscular (IM) administration, so as to prevent the worsening of presarcopenia or even recover from the early stage of the illness. In this research, BSP-HAP was synthesized by a modified low temperature co-precipitation process that would be beneficial for BSP loading. By conducting DCFDA, WST-1 and the Live/Dead assay, BSP-HAP is shown to be a biocompatible material which may release BSP by cells through the endocytosis pathway. Animal studies revealed that the rats treated with BSP-HAP could effectively recover muscle endurance, grip strength or fat/lean mass ratio from lipopolysaccharide (LPS)-induced sarcopenia. This study shows BSP delivered by BSP-HAP system has potential for application in the treatment and prevention of sarcopenia in the future. Full article
(This article belongs to the Special Issue Oxidative Stress in Skeletal Muscle)
►▼ Show Figures

Figure 1

24 pages, 4565 KiB  
Article
Nitrosative Redox Homeostasis and Antioxidant Response Defense in Disused Vastus lateralis Muscle in Long-Term Bedrest (Toulouse Cocktail Study)
by Dieter Blottner, Daniele Capitanio, Gabor Trautmann, Sandra Furlan, Guido Gambara, Manuela Moriggi, Katharina Block, Pietro Barbacini, Enrica Torretta, Guillaume Py, Angèle Chopard, Imre Vida, Pompeo Volpe, Cecilia Gelfi and Michele Salanova
Antioxidants 2021, 10(3), 378; https://doi.org/10.3390/antiox10030378 - 3 Mar 2021
Cited by 14 | Viewed by 3300
Abstract
Increased oxidative stress by reactive oxygen species (ROS) and reactive nitrogen species (RNS) is a major determinant of disuse-induced muscle atrophy. Muscle biopsies (thigh vastus lateralis, VL) obtained from healthy male subjects enrolled in the Toulouse Cocktail bedrest (BR) study were used [...] Read more.
Increased oxidative stress by reactive oxygen species (ROS) and reactive nitrogen species (RNS) is a major determinant of disuse-induced muscle atrophy. Muscle biopsies (thigh vastus lateralis, VL) obtained from healthy male subjects enrolled in the Toulouse Cocktail bedrest (BR) study were used to assess efficacy of an antioxidant cocktail (polyphenols, omega-3, vitamin E, and selenium) to counteract the increased redox homeostasis and enhance the antioxidant defense response by using label-free LC–MS/MS and NITRO-DIGE (nitrosated proteins), qPCR, and laser confocal microscopy. Label-free LC–MS/MS indicated that treatment prevented the redox homeostasis dysregulation and promoted structural remodeling (TPM3, MYH7, MYBPC, MYH1, MYL1, HRC, and LUM), increment of RyR1, myogenesis (CSRP3), and skeletal muscle development (MUSTN1, LMNA, AHNAK). These changes were absent in the Placebo group. Glycolysis, tricarboxylic acid cycle (TCA), oxidative phosphorylation, fatty acid beta-oxidation, and mitochondrial transmembrane transport were normalized in treated subjects. Proteins involved in protein folding were also normalized, whereas protein entailed in ion homeostasis decreased. NITRO-DIGE analysis showed significant protein nitrosylation changes for CAT, CA3, SDHA, and VDAC2 in Treatment vs. Placebo. Similarly, the nuclear factor erythroid 2-related factor 2 (Nrf-2) antioxidant response element (Nrf-2 ARE) signaling pathway showed an enhanced response in the Treatment group. Increased nitrosative redox homeostasis and decreased antioxidant defense response were found in post-BR control (Placebo, n = 10) vs. the antioxidant cocktail treated group (Treatment, n = 10). Taken together, increased nitrosative redox homeostasis and muscle deterioration during BR-driven physical inactivity were prevented, whereas decreased antioxidant nitrosative stress defense response was attenuated by Treatment suggesting positive effects of the nutritional intervention protocol in bedrest. Full article
(This article belongs to the Special Issue Oxidative Stress in Skeletal Muscle)
►▼ Show Figures

Figure 1

15 pages, 1353 KiB  
Article
Oxidative Stress in Endurance Cycling Is Reduced Dose-Dependently after One Month of Re-Esterified DHA Supplementation
by Lydia de Salazar, Carlos Contreras, Antonio Torregrosa-García, Antonio J. Luque-Rubia, Vicente Ávila-Gandía, Joan Carles Domingo and Francisco Javier López-Román
Antioxidants 2020, 9(11), 1145; https://doi.org/10.3390/antiox9111145 - 18 Nov 2020
Cited by 8 | Viewed by 3267 | Correction
Abstract
Docosahexaenoic acid (DHA) supplementation can reduce exercise-induced oxidative stress generated during long aerobic exercise, with the minimum dose yet to be elucidated for physically active subjects. In this study, we performed a dose finding with re-esterified DHA in triglyceride form in a randomized [...] Read more.
Docosahexaenoic acid (DHA) supplementation can reduce exercise-induced oxidative stress generated during long aerobic exercise, with the minimum dose yet to be elucidated for physically active subjects. In this study, we performed a dose finding with re-esterified DHA in triglyceride form in a randomized double-blind parallel trial at different doses (350, 1050, 1750, and 2450 mg a day) for 4 weeks in males engaged in regular cycling (n = 100, 7.6 ± 3.7 h/week). The endogenous antioxidant capacity of DHA was quantified as a reduction in the levels of the oxidative stress marker 8-hydroxy-2′-deoxyguanosine (8-OHdG) recollected in 24-h urine samples after 90 min of constant load cycling before and after intervention. To ascertain incorporation of DHA, erythrocyte polyunsaturated fatty acid (PUFA) composition was compared along groups. We found a dose-dependent antioxidant capacity of DHA from 1050 mg with a trend to neutralization for the highest dose of 2450 mg (placebo: n = 13, F = 0.041; 350 mg: n = 10, F = 0.268; 1050 mg: n = 11, F = 7.112; 1750 mg: n = 12, F = 9.681; 2450 mg: n = 10, F = 15.230). In the erythrocyte membrane, the re-esterified DHA increased DHA and omega-3 percentage and decreased omega 6 and the omega-6 to omega-3 ratio, while Eicosapentaenoic acid (EPA) and PUFA remained unchanged. Supplementation of re-esterified DHA exerts a dose-dependent endogenous antioxidant property against moderate-intensity long-duration aerobic exercise in physically active subjects when provided at least 1050 mg a day for 4 weeks. Full article
(This article belongs to the Special Issue Oxidative Stress in Skeletal Muscle)
►▼ Show Figures

Graphical abstract

Review

Jump to: Editorial, Research

17 pages, 1517 KiB  
Review
H2O2/Ca2+/Zn2+ Complex Can Be Considered a “Collaborative Sensor” of the Mitochondrial Capacity?
by Ester Sara Di Filippo, Franco Checcaglini, Giorgio Fanò-Illic and Stefania Fulle
Antioxidants 2022, 11(2), 342; https://doi.org/10.3390/antiox11020342 - 9 Feb 2022
Cited by 7 | Viewed by 2028
Abstract
In order to maintain a state of well-being, the cell needs a functional control center that allows it to respond to changes in the internal and surrounding environments and, at the same time, carry out the necessary metabolic functions. In this review, we [...] Read more.
In order to maintain a state of well-being, the cell needs a functional control center that allows it to respond to changes in the internal and surrounding environments and, at the same time, carry out the necessary metabolic functions. In this review, we identify the mitochondrion as such an “agora”, in which three main messengers are able to collaborate and activate adaptive response mechanisms. Such response generators, which we have identified as H2O2, Ca2+, and Zn2+, are capable of “reading” the environment and talking to each other in cooperation with the mitochondrion. In this manner, these messengers exchange information and generate a holistic response of the whole cell, dependent on its functional state. In this review, to corroborate this claim, we analyzed the role these actors, which in the review we call “sensors”, play in the regulation of skeletal muscle contractile capacities chosen as a model of crosstalk between Ca2+, Zn2+, and H2O2. Full article
(This article belongs to the Special Issue Oxidative Stress in Skeletal Muscle)
►▼ Show Figures

Figure 1

30 pages, 1407 KiB  
Review
Beneficial Role of Exercise in the Modulation of mdx Muscle Plastic Remodeling and Oxidative Stress
by Monica Frinchi, Giuseppe Morici, Giuseppa Mudó, Maria R. Bonsignore and Valentina Di Liberto
Antioxidants 2021, 10(4), 558; https://doi.org/10.3390/antiox10040558 - 3 Apr 2021
Cited by 11 | Viewed by 3512
Abstract
Duchenne muscular dystrophy (DMD) is an X-linked recessive progressive lethal disorder caused by the lack of dystrophin, which determines myofibers mechanical instability, oxidative stress, inflammation, and susceptibility to contraction-induced injuries. Unfortunately, at present, there is no efficient therapy for DMD. Beyond several promising [...] Read more.
Duchenne muscular dystrophy (DMD) is an X-linked recessive progressive lethal disorder caused by the lack of dystrophin, which determines myofibers mechanical instability, oxidative stress, inflammation, and susceptibility to contraction-induced injuries. Unfortunately, at present, there is no efficient therapy for DMD. Beyond several promising gene- and stem cells-based strategies under investigation, physical activity may represent a valid noninvasive therapeutic approach to slow down the progression of the pathology. However, ethical issues, the limited number of studies in humans and the lack of consistency of the investigated training interventions generate loss of consensus regarding their efficacy, leaving exercise prescription still questionable. By an accurate analysis of data about the effects of different protocol of exercise on muscles of mdx mice, the most widely-used pre-clinical model for DMD research, we found that low intensity exercise, especially in the form of low speed treadmill running, likely represents the most suitable exercise modality associated to beneficial effects on mdx muscle. This protocol of training reduces muscle oxidative stress, inflammation, and fibrosis process, and enhances muscle functionality, muscle regeneration, and hypertrophy. These conclusions can guide the design of appropriate studies on human, thereby providing new insights to translational therapeutic application of exercise to DMD patients. Full article
(This article belongs to the Special Issue Oxidative Stress in Skeletal Muscle)
►▼ Show Figures

Graphical abstract

29 pages, 1305 KiB  
Review
How N-Acetylcysteine Supplementation Affects Redox Regulation, Especially at Mitohormesis and Sarcohormesis Level: Current Perspective
by Aslı Devrim-Lanpir, Lee Hill and Beat Knechtle
Antioxidants 2021, 10(2), 153; https://doi.org/10.3390/antiox10020153 - 21 Jan 2021
Cited by 11 | Viewed by 5630
Abstract
Exercise frequently alters the metabolic processes of oxidative metabolism in athletes, including exposure to extreme reactive oxygen species impairing exercise performance. Therefore, both researchers and athletes have been consistently investigating the possible strategies to improve metabolic adaptations to exercise-induced oxidative stress. N-acetylcysteine (NAC) [...] Read more.
Exercise frequently alters the metabolic processes of oxidative metabolism in athletes, including exposure to extreme reactive oxygen species impairing exercise performance. Therefore, both researchers and athletes have been consistently investigating the possible strategies to improve metabolic adaptations to exercise-induced oxidative stress. N-acetylcysteine (NAC) has been applied as a therapeutic agent in treating many diseases in humans due to its precursory role in the production of hepatic glutathione, a natural antioxidant. Several studies have investigated NAC’s possible therapeutic role in oxidative metabolism and adaptive response to exercise in the athletic population. However, still conflicting questions regarding NAC supplementation need to be clarified. This narrative review aims to re-evaluate the metabolic effects of NAC on exercise-induced oxidative stress and adaptive response developed by athletes against the exercise, especially mitohormetic and sarcohormetic response. Full article
(This article belongs to the Special Issue Oxidative Stress in Skeletal Muscle)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-9
Back to TopTop