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 2496

Special Issue Editors


E-Mail Website
Guest Editor
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
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
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

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

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

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
Viewed by 1791
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)
Show Figures

Figure 1

Back to TopTop