Role of Skeletal Muscle and Exercise in Oxidative Stress-Related Diseases

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 (28 February 2026) | Viewed by 2140

Special Issue Editor


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Guest Editor
Department of Rehabilitation, R Professional University of Rehabilitation, 2-10-35 Kohoku, Tsuchiura 300-0032, Japan
Interests: exercise; muscle quality; nonalcoholic fatty liver disease; type 2 diabetes; oxidative stress

Special Issue Information

Dear Colleagues,

We invite researchers, clinicians, and interdisciplinary experts to contribute original research articles, comprehensive reviews, and short communications to this Special Issue.

Oxidative stress plays a key role in the development of many chronic diseases, including metabolic syndrome, nonalcoholic fatty liver disease, type 2 diabetes, cardiovascular disorders, sarcopenia, and neurodegenerative conditions. Skeletal muscle, which is highly metabolically active and rich in redox-sensitive pathways, is a central target and active regulator of systemic oxidative stress. Exercise is a non-pharmacological intervention that provides significant benefits by influencing redox homeostasis, muscle adaptation, and systemic health. This makes exercise a promising area of research for disease prevention and management.

This Special Issue aims to explore and expand knowledge across the following key areas:

(1) The molecular and cellular mechanisms by which oxidative stress affects skeletal muscle function, regeneration, and degeneration, including mitochondrial dysfunction, redox signaling, inflammation, proteostasis imbalance, and apoptosis.

(2) Exercise-induced adaptations in skeletal muscle under oxidative stress conditions, such as mitochondrial biogenesis, antioxidant responses, muscle-fiber-type switching, autophagy, and hormetic regulation.

(3) The identification of novel biomarkers, therapeutic targets, and regulatory pathways connecting oxidative stress to muscle health has implications for diagnosis, prognosis, and personalized interventions.

(4) Translational and clinical perspectives on the modulation of muscle physiology by redox, especially in aging populations, patients with chronic diseases, and individuals with varying physical activity levels.

(5) Comparative analysis of the effects of different exercise modalities, including endurance, resistance, and high-intensity interval training, on skeletal muscle redox status and functional outcomes in health and disease contexts.

(6) The development of integrated therapeutic strategies combining exercise with pharmacological or nutritional approaches to optimize oxidative stress control and promote muscle health.

We welcome multidisciplinary contributions from the fields of molecular biology, physiology, clinical research, biochemistry, sports science, rehabilitation, and public health.

Prof. Dr. Sechang Oh
Guest Editor

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Keywords

  • oxidative stress
  • skeletal muscle
  • exercise
  • physical activity
  • redox biology
  • chronic disease prevention
  • muscle adaptation
  • biomarkers of oxidative stress

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Published Papers (1 paper)

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Research

20 pages, 1888 KB  
Article
N-Acetylcysteine Prevents Skeletal Muscle Cisplatin-Induced Atrophy by Inducing Myogenic microRNAs and Maintaining the Redox Balance
by Teminijesu Dorcas Aremu, Tonali Blanco Ayala, Karla F. Meza-Sosa, Daniela Ramírez Ortega, Dinora F. González Esquivel, Gustavo I. Vázquez Cervantes, Itamar Flores, Wendy Leslie González Alfonso, Verónica Custodio Ramírez, Alelí Salazar, Benjamin Pineda, Gonzalo Pérez de la Cruz, Saul Gómez Manzo, Gabriel Roldan Roldan, Paul Carrillo Mora and Verónica Pérez de la Cruz
Antioxidants 2025, 14(11), 1344; https://doi.org/10.3390/antiox14111344 - 8 Nov 2025
Cited by 1 | Viewed by 1735
Abstract
Cisplatin (CIS) is a widely used chemotherapeutic agent known for its efficacy; however, it induces several adverse effects, most notably cachexia, which is characterized by progressive loss of skeletal muscle mass, weakness, and reduced body weight. N-acetylcysteine (NAC) a compound with antioxidants properties, [...] Read more.
Cisplatin (CIS) is a widely used chemotherapeutic agent known for its efficacy; however, it induces several adverse effects, most notably cachexia, which is characterized by progressive loss of skeletal muscle mass, weakness, and reduced body weight. N-acetylcysteine (NAC) a compound with antioxidants properties, has been shown to mitigate CIS-induced neurotoxicity in experimental models. This study aimed to investigate the myoprotective effects of NAC during CIS treatment and explore the redox and molecular mechanisms involved in this response. For this, female Wistar rats were divided into four experimental groups: Control, NAC (300 mg/day/8 days), CIS (3 mg/kg i.p for 5 days), and NAC + CIS (NAC for 8 days, with CIS administered from day 4 onward). After treatment, muscle strength, redox status, mitochondrial biogenesis, expression of myogenic microRNAs and morphological changes were evaluated. CIS treatment caused muscle atrophy, decreased GSH/GSSG ratio, impaired cellular function, increased lipid peroxidation and altered antioxidant enzymes activity. These effects were mitigated by NAC coadministration. CIS also reduced the mtDNA/nDNA ratio; however, NAC treatment tended to increase TFAM and PGC-1α expression levels. Furthermore, CIS suppressed the expression of muscular miR-1-3p, miR-133a-3p and miR-206-3p, while NAC restored their levels when co-administered with CIS. These findings suggest that NAC may serve as a promising adjuvant therapeutic strategy to counteract CIS-induced myotoxicity through redox regulation and modulation of molecular pathways related to muscle integrity and regeneration. Full article
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