Exploring the Role of Redox Biology in Skeletal Muscle-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 (31 March 2024) | Viewed by 1486

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Department of Health and Kinesiology, Graduate Faculty of Nutrition, Texas A&M University, College Station, TX, USA
Interests: microgravity environments; cell biology; oxidative stress; skeletal muscle
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Special Issue Information

Dear Colleagues,

Skeletal muscle, a highly dynamic and essential tissue, plays a fundamental role in locomotion, posture, metabolism, and overall human health. However, various diseases and conditions can disrupt the normal functioning of skeletal muscle, leading to significant impairments in mobility and quality of life. Over the years, extensive research has focused on unraveling the complex mechanisms underlying skeletal muscle-related diseases, with a particular emphasis on understanding the involvement of redox biology. Redox biology, the study of oxidative and reductive processes in biological systems, has emerged as a critical field in understanding the pathophysiology of various diseases. In the context of skeletal muscle, redox biology encompasses the intricate interplay between oxidative stress and antioxidant defense mechanisms, as well as the involvement of reactive oxygen species (ROS), reactive nitrogen species (RNS), and their impact on cellular signaling pathways.

This special issue of the Antioxidant Journal aims to explore the significant contributions of redox biology in elucidating the molecular mechanisms underlying skeletal muscle-related diseases. By highlighting recent advancements and breakthroughs in the field, we aim to provide a comprehensive overview of the role of oxidative stress and redox signaling in the pathogenesis of skeletal muscle disorders and potential therapeutic strategies targeting redox homeostasis. We encourage submissions that offer novel insights and contribute to advancing the field's understanding of cellular and molecular mechanisms involved in these disorders. 

The scope of this special issue encompasses a wide range of skeletal muscle-related diseases, including, but not limited to, muscular dystrophies, sarcopenia, diabetes, myopathies, spaceflight, and exercise-induced muscle damage. We welcome research articles, review articles, and perspective pieces that delve into redox biology's molecular and cellular aspects and its relevance to skeletal muscle health and disease. 

Key topics of interest for this special issue include, but are not limited to:

  • Mechanisms of oxidative stress in skeletal muscle-related diseases.
  • Redox signaling pathways and their impact on muscle regeneration and repair.
  • Role of antioxidant defenses in skeletal muscle protection.
  • The influence of exercise and physical activity on redox homeostasis in muscle.
  • Emerging therapeutic strategies targeting redox imbalance in skeletal muscle disorders.
  • Biomarkers of oxidative stress and redox status in skeletal muscle-related diseases.
  • Novel experimental models and methodologies to study redox biology in skeletal muscle.
  • Nutritional interventions and dietary antioxidants in the management of skeletal muscle diseases.

We encourage researchers from diverse disciplines, including but not limited to biochemistry, molecular biology, physiology, pharmacology, and clinical medicine, to contribute to this special issue. By bringing together a collection of high-quality research and reviews, we aim to foster interdisciplinary collaborations and advance our understanding of the intricate relationship between redox biology and skeletal muscle-related diseases.

We look forward to receiving your valuable contributions to this special issue of the Antioxidant Journal, fostering collaborative discussions and advancing the field of redox biology in skeletal muscle-related diseases.

Dr. Khaled Kamal
Prof. Dr. John Lawler
Guest Editors

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Published Papers (1 paper)

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Research

16 pages, 2783 KiB  
Article
Oxidised Albumin Levels in Plasma and Skeletal Muscle as Biomarkers of Disease Progression and Treatment Efficacy in Dystrophic mdx Mice
by Jessica R. Terrill, Angelo Patrick R. Bautista, Irene Tsioutsias, Miranda D. Grounds and Peter G. Arthur
Antioxidants 2024, 13(6), 720; https://doi.org/10.3390/antiox13060720 - 13 Jun 2024
Viewed by 1155
Abstract
Redox modifications to the plasma protein albumin have the potential to be used as biomarkers of disease progression and treatment efficacy in pathologies associated with inflammation and oxidative stress. One such pathology is Duchenne muscular dystrophy (DMD), a fatal childhood disease characterised by [...] Read more.
Redox modifications to the plasma protein albumin have the potential to be used as biomarkers of disease progression and treatment efficacy in pathologies associated with inflammation and oxidative stress. One such pathology is Duchenne muscular dystrophy (DMD), a fatal childhood disease characterised by severe muscle wasting. We have previously shown in the mdx mouse model of DMD that plasma albumin thiol oxidation is increased; therefore, the first aim of this paper was to establish that albumin thiol oxidation in plasma reflects levels within mdx muscle tissue. We therefore developed a method to measure tissue albumin thiol oxidation. We show that albumin thiol oxidation was increased in both mdx muscle and plasma, with levels correlated with measures of dystropathology. In dystrophic muscle, albumin content was associated with areas of myonecrosis. The second aim was to test the ability of plasma thiol oxidation to track acute changes in dystropathology: we therefore subjected mdx mice to a single treadmill exercise session (known to increase myonecrosis) and took serial blood samples. This acute exercise caused a transient increase in total plasma albumin oxidation and measures of dystropathology. Together, these data support the use of plasma albumin thiol oxidation as a biomarker to track active myonecrosis in DMD. Full article
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