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Antioxidants
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Redox and Inflammatory Regulation of Skeletal Muscle Mass and Function...
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Redox and Inflammatory Regulation of Skeletal Muscle Mass and Function in Health and Disease

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: 30 April 2025 | Viewed by 3650

Special Issue Editor

Prof. Dr. Claudio Cabello-Verrugio

E-Mail Website
Guest Editor
Departamento de Ciencias Biológicas, Facultad de Ciencias de la Vida, Universidad Andres Bello, Santiago, Chile
Interests: primary and secondary sarcopenia; bile acids; satellite cells; fibrosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The numbers of people affected by non-transmissible chronic diseases and aging have increased in recent years and among the critical causes of these pathological states are inflammation and oxidative stress, imbalances between the formation of oxidant species, such as reactive oxygen species (ROS) and reactive nitrogen species (RNS), and antioxidant mechanisms. Many tissues, among them skeletal muscle, are exposed to oxidative stress and inflammation with harmful biological effects of ROS and inflammatory cytokines, such as alteration of muscle function and physiology. ROS can regulate several redox-sensitive signaling pathways that play a critical role in gene expression or protein modification. While oxidant species and inflammatory signals have gained much attention for their harmful effects on muscle contractibility, fatigue, and metabolic dysfunction, research has also shown ROS to facilitate muscle adaptation after stressors such as physical exercise.

We invite researchers and scientists to apply and contribute original research and review articles that reflect the progress in elucidating the mechanisms of the balance between ROS and cellular antioxidant machinery, their relationships with inflammation, and how they may be altered during muscle pathologies, emphasizing aging and chronic diseases. We welcome all articles that describe new and essential findings on the roles of oxidative stress and inflammation in sarcopenia, cachexia, myopathies, or any other muscle dysfunction. Submissions are expected that enable the expanding of knowledge and describe new strategies to treat or prevent a pathological status in which oxidative stress might be involved.

Prof. Dr. Claudio Cabello-Verrugio
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

  • skeletal muscle
  • oxidative stress
  • sarcopenia
  • inflammation
  • ROS
  • redox signaling

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Published Papers (3 papers)

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22 pages, 4057 KiB  
Article
CCL5 Induces a Sarcopenic-like Phenotype via the CCR5 Receptor
by Francisco Aguirre, Franco Tacchi, Mayalen Valero-Breton, Josué Orozco-Aguilar, Sabrina Conejeros-Lillo, Josefa Bonicioli, Renata Iturriaga-Jofré, Daniel Cabrera, Jorge A. Soto, Mauricio Castro-Sepúlveda, Marianny Portal-Rodríguez, Álvaro A. Elorza, Andrea Matamoros, Felipe Simon and Claudio Cabello-Verrugio
Antioxidants 2025, 14(1), 84; https://doi.org/10.3390/antiox14010084 - 13 Jan 2025
Viewed by 634
Abstract
Sarcopenia corresponds to a decrease in muscle mass and strength. CCL5 is a new myokine whose expression, along with the CCR5 receptor, is increased in sarcopenic muscle. Therefore, we evaluated whether CCL5 and CCR5 induce a sarcopenic-like effect on skeletal muscle tissue and [...] Read more.
Sarcopenia corresponds to a decrease in muscle mass and strength. CCL5 is a new myokine whose expression, along with the CCR5 receptor, is increased in sarcopenic muscle. Therefore, we evaluated whether CCL5 and CCR5 induce a sarcopenic-like effect on skeletal muscle tissue and cultured muscle cells. Electroporation in the tibialis anterior (TA) muscle of mice was used to overexpress CCL5. The TA muscles were analyzed by measuring the fiber diameter, the content of sarcomeric proteins, and the gene expression of E3-ligases. C2C12 myotubes and single-isolated flexor digitorum brevis (FDB) fibers were also treated with recombinant CCL5 (rCCL5). The participation of CCR5 was evaluated using the antagonist maraviroc (MVC). Protein and structural analyses were performed. The results showed that TA overexpression of CCL5 led to sarcopenia by reducing muscle strength and mass, muscle-fiber diameter, and sarcomeric protein content, and by upregulating E3-ligases. The same sarcopenic phenotype was observed in myotubes and FDB fibers. We showed increased reactive oxygen species (ROS) production and carbonylated proteins, denoting oxidative stress induced by CCL5. When the CCR5 was antagonized, the effects produced by rCCL5 were prevented. In conclusion, we report for the first time that CCL5 is a novel myokine that exerts a sarcopenic-like effect through the CCR5 receptor. Full article
(This article belongs to the Special Issue Redox and Inflammatory Regulation of Skeletal Muscle Mass and Function in Health and Disease)
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17 pages, 5284 KiB  
Article
Accelerated Sarcopenia Phenotype in the DJ-1/Park7-Knockout Zebrafish
by Kristine O. Rostad, Tobias Trognitz, Ann Kristin Frøyset, Ersilia Bifulco and Kari E. Fladmark
Antioxidants 2024, 13(12), 1509; https://doi.org/10.3390/antiox13121509 - 11 Dec 2024
Viewed by 986
Abstract
Age-dependent loss of muscle mass and function is associated with oxidative stress. DJ-1/Park7 acts as an antioxidant through multiple signalling pathways. DJ-1-knockout zebrafish show a decline in swimming performance and loss of weight gain between 6 and 9 months of age. Here, [...] Read more.
Age-dependent loss of muscle mass and function is associated with oxidative stress. DJ-1/Park7 acts as an antioxidant through multiple signalling pathways. DJ-1-knockout zebrafish show a decline in swimming performance and loss of weight gain between 6 and 9 months of age. Here, we address the degree to which this is associated with muscle degeneration and identify molecular changes preceding dysregulation of muscle performance. Loss of DJ-1 reduced the skeletal muscle fibre cross-section area. The highly mitochondrial-dependent red slow muscle was more affected than the white muscle, and degeneration of sub-sarcolemma red muscle mitochondria was observed. Using TandemMassTag-based quantitative proteomics, we identified a total of 3721 proteins in the multiplex sample of 4 and 12-month-old muscles. A total of 68 proteins, mainly associated with inflammation and mitochondrial function, were dysregulated in the young DJ-1-null adults, with Annexin A3, Sphingomyelin phosphodiesterase acid-like 3B, Complement C3a, and 2,4-dienoyl CoA reductase 1 being the most affected. The loss of DJ-1 also accelerated molecular features associated with sarcopenia, such as a decrease in the NAD+/NADH ratio and a reduction in Prostaglandin reductase 2 and Cytosolic glycerol-3-phosphate dehydrogenase levels. In view of the experimental power of zebrafish, the DJ-1-null zebrafish makes a valuable model for understanding the connection between oxidative stress and age-dependent muscle loss and function. Full article
(This article belongs to the Special Issue Redox and Inflammatory Regulation of Skeletal Muscle Mass and Function in Health and Disease)
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5 pages, 3083 KiB  
Commentary
The Double-Edged Sword of ROS in Muscle Wasting and COPD: Insights from Aging-Related Sarcopenia
by S. M. H. Chan, S. Selemidis and R. Vlahos
Antioxidants 2024, 13(7), 882; https://doi.org/10.3390/antiox13070882 - 22 Jul 2024
Viewed by 1475
Abstract
An elevation in reactive oxygen species (ROS) is widely accepted to be a key mechanism that drives chronic obstructive pulmonary disease (COPD) and its major co-morbidity, skeletal muscle wasting. However, it will be perhaps a surprise to many that an elevation in ROS [...] Read more.
An elevation in reactive oxygen species (ROS) is widely accepted to be a key mechanism that drives chronic obstructive pulmonary disease (COPD) and its major co-morbidity, skeletal muscle wasting. However, it will be perhaps a surprise to many that an elevation in ROS in skeletal muscle is also a critical process for normal skeletal muscle function and in the adaptations to physical exercise. The key message here is that ROS are not solely detrimental. This duality of ROS suggests that the mere use of a broad-acting antioxidant is destined to fail in alleviating skeletal muscle wasting in COPD because it will also be influencing critical physiological ROS-dependent processes. Here, we take a close look at this duality of ROS in skeletal muscle physiology and pathophysiology pertaining to COPD and will aim to gain critical insights from other skeletal muscle wasting conditions due to aging such as sarcopenia. Full article
(This article belongs to the Special Issue Redox and Inflammatory Regulation of Skeletal Muscle Mass and Function in Health and Disease)
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