Antioxidants and Oxidative Stress: Implication in Muscle 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 December 2023) | Viewed by 3088

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Department of Biomedical, Experimental and Clinical Sciences “Mario Serio”, University of Florence, Viale Morgagni 50, 50134 Florence, Italy
Interests: redox markers; antioxidant capacity; post-translational oxidative modification; ROS sources
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Guest Editor
Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Firenze, 50121 Firenze, Italy
Interests: thrombosis; fibrinogen; oxidative stress; protein structure
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Reactive Oxygen Species (ROS) represent fundamental key players in a large variety of physiological mechanisms. However, despite the development of a composite antioxidant system, their excessive levels can establish oxidative stress, a condition which is responsible for the initiation and progression of tissue/organ injury. The role of oxidative stress in muscle homeostasis is quite intricate and far to be elucidated. Within physiological levels ROS exert essential actions in muscle homeostasis by regulating excitation-contraction coupling, growth, proliferation, differentiation and muscle adaptation. The underlying mechanisms are represented by ROS interactions with redox-sensitive transcription factors, leading to increased gene expression of antioxidant enzymes, cytoprotective proteins and other enzymes involved in muscle specific metabolic functions.

Nevertheless, an uncontrolled ROS accumulation displays many deleterious effects such as a reduction in force generation and an increase in muscle atrophy. In particular, excessive ROS levels can activate distinct pathogenic pathways thus triggering pathological conditions and accelerating aging.

At muscular level, several studies suggested that transiently increased ROS levels, which might be consequent to muscle activity, on one hand can enhance body’s antioxidant defense systems thus reflecting a potentially health promoting process, on the other hand, can be responsible for the onset of oxidative stress whose pathological consequences could be counterbalanced by redox balancing treatments. Additional studies are therefore necessary to highlight whether the manipulation of redox balance can represent a valuable tool in the design of therapeutic strategies for muscle diseases. In this context it is mandatory to determine the utility of antioxidant supplementation considering fundamental aspects such as type, dose and duration of antioxidant supplementation.

On these bases, we invite you to submit your latest research findings or a review article to this Special Issue, which will be focused on antioxidants and oxidative stress in muscle diseases. Both in vitro and in vivo studies relating to these topics will be suitable for the current issue. We look forward to your contribution.

Dr. Claudia Fiorillo
Dr. Matteo Becatti
Guest Editors

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Keywords

  • oxidative stress
  • antioxidants
  • muscle
  • muscle disease
  • redox markers
  • redox signaling lipid peroxidation

Published Papers (2 papers)

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Research

17 pages, 2961 KiB  
Article
A Novel MAO-B/SSAO Inhibitor Improves Multiple Aspects of Dystrophic Phenotype in mdx Mice
by Francesca Gasparella, Leonardo Nogara, Elena Germinario, Lucia Tibaudo, Stefano Ciciliot, Giorgia Piccoli, Francisca Carolina Venegas, Francesca Fontana, Gabriele Sales, Daniele Sabbatini, Jonathan Foot, Wolfgang Jarolimek, Bert Blaauw, Marcella Canton and Libero Vitiello
Antioxidants 2024, 13(6), 622; https://doi.org/10.3390/antiox13060622 - 21 May 2024
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Abstract
Duchenne muscular dystrophy (DMD) is one of the most frequent and severe childhood muscle diseases. Its pathophysiology is multifaceted and still incompletely understood, but we and others have previously shown that oxidative stress plays an important role. In particular, we have demonstrated that [...] Read more.
Duchenne muscular dystrophy (DMD) is one of the most frequent and severe childhood muscle diseases. Its pathophysiology is multifaceted and still incompletely understood, but we and others have previously shown that oxidative stress plays an important role. In particular, we have demonstrated that inhibition of mitochondrial monoamine oxidases could improve some functional and biohumoral markers of the pathology. In the present study we report the use of dystrophic mdx mice to evaluate the efficacy of a dual monoamine oxidase B (MAO-B)/semicarbazide-sensitive amine oxidase (SSAO) inhibitor, PXS-5131, in reducing inflammation and fibrosis and improving muscle function. We found that a one-month treatment starting at three months of age was able to decrease reactive oxygen species (ROS) production, fibrosis, and inflammatory infiltrate in the tibialis anterior (TA) and diaphragm muscles. Importantly, we also observed a marked improvement in the capacity of the gastrocnemius muscle to maintain its force when challenged with eccentric contractions. Upon performing a bulk RNA-seq analysis, PXS-5131 treatment affected the expression of genes involved in inflammatory processes and tissue remodeling. We also studied the effect of prolonged treatment in older dystrophic mice, and found that a three-month administration of PXS-5131 was able to greatly reduce the progression of fibrosis not only in the diaphragm but also in the heart. Taken together, these results suggest that PXS-5131 is an effective inhibitor of fibrosis and inflammation in dystrophic muscles, a finding that could open a new therapeutic avenue for DMD patients. Full article
(This article belongs to the Special Issue Antioxidants and Oxidative Stress: Implication in Muscle Diseases)
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31 pages, 9245 KiB  
Article
Actin Polymerization Defects Induce Mitochondrial Dysfunction in Cellular Models of Nemaline Myopathies
by Rocío Piñero-Pérez, Alejandra López-Cabrera, Mónica Álvarez-Córdoba, Paula Cilleros-Holgado, Marta Talaverón-Rey, Alejandra Suárez-Carrillo, Manuel Munuera-Cabeza, David Gómez-Fernández, Diana Reche-López, Ana Romero-González, José Manuel Romero-Domínguez, Rocío M. de Pablos and José A. Sánchez-Alcázar
Antioxidants 2023, 12(12), 2023; https://doi.org/10.3390/antiox12122023 - 21 Nov 2023
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Abstract
Nemaline myopathy (NM) is one of the most common forms of congenital myopathy and it is identified by the presence of “nemaline bodies” (rods) in muscle fibers by histopathological examination. The most common forms of NM are caused by mutations in the Actin [...] Read more.
Nemaline myopathy (NM) is one of the most common forms of congenital myopathy and it is identified by the presence of “nemaline bodies” (rods) in muscle fibers by histopathological examination. The most common forms of NM are caused by mutations in the Actin Alpha 1 (ACTA1) and Nebulin (NEB) genes. Clinical features include hypotonia and muscle weakness. Unfortunately, there is no curative treatment and the pathogenetic mechanisms remain unclear. In this manuscript, we examined the pathophysiological alterations in NM using dermal fibroblasts derived from patients with mutations in ACTA1 and NEB genes. Patients’ fibroblasts were stained with rhodamine–phalloidin to analyze the polymerization of actin filaments by fluorescence microscopy. We found that patients’ fibroblasts showed incorrect actin filament polymerization compared to control fibroblasts. Actin filament polymerization defects were associated with mitochondrial dysfunction. Furthermore, we identified two mitochondrial-boosting compounds, linoleic acid (LA) and L-carnitine (LCAR), that improved the formation of actin filaments in mutant fibroblasts and corrected mitochondrial bioenergetics. Our results indicate that cellular models can be useful to study the pathophysiological mechanisms involved in NM and to find new potential therapies. Furthermore, targeting mitochondrial dysfunction with LA and LCAR can revert the pathological alterations in NM cellular models. Full article
(This article belongs to the Special Issue Antioxidants and Oxidative Stress: Implication in Muscle Diseases)
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