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Antioxidants
Special Issues
Mitochondrial Functions and Oxidative Stress during Cardiorespiratory and Muscular Diseases
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Mitochondrial Functions and Oxidative Stress during Cardiorespiratory and Muscular 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 (15 March 2023) | Viewed by 15126

Special Issue Editors

Dr. Bernard Geny

E-Mail Website
Guest Editor
1. Team 3072 “Mitochondria, Oxidative Stress and Muscle Protection”, Translational Medicine Federation of Strasbourg (FMTS), Faculty of Medicine, University of Strasbourg, 11 Rue Humann, 67000 Strasbourg, France
2. Physiology and Functional Exploration Service, University Hospital of Strasbourg, 1 Place de l’Hôpital, 67091 Strasbourg, France
Interests: antioxidants; oxidative stress; mitochondria; skeletal muscles
Special Issues, Collections and Topics in MDPI journals
Dr. Marianne Riou

E-Mail Website
Guest Editor
1. Team 3072 “Mitochondria, Oxidative Stress and Muscle Protection”, Translational Medicine Federation of Strasbourg (FMTS), Faculty of Medicine, University of Strasbourg, 11 Rue Humann, 67000 Strasbourg, France
2. Physiology and Functional Exploration Service, University Hospital of Strasbourg, 1 Place de l’Hôpital, 67091 Strasbourg, France
Interests: pulmonary artery hypertension (PAH) pathophysiology (including PBMCs rôle in PAH); diagnostic and therapy

Special Issue Information

Dear Colleagues,

Peripheral blood mononuclear cells (PBMCs) are involved in many inflammatory diseases, and recent data support that the mitochondrial alterations in PBMCs might play key roles in cardiovascular, muscular, and respiratory diseases. However, COVID-19 infection, similar to sepsis, modifies the mitochondrial respiration PBMCs. Accordingly, mitochondria are largely involved in cell energy and in the production of reactive oxygen species (ROSs), which can act as either useful signaling factors or lead to protein, lipid, and DNA damage as well as tissue dysfunction.

Mitochondrial dysfunction, including decreased oxidative capacity and impaired calcium handling, are potentially associated with abnormal mitochondrial dynamics and have been reported in cardiac, pulmonary, and muscle tissues. PBMCs have also been found to be associated with the severity of cardiac failure.

It is important to introduce new perspectives on the pathophysiology of such public health issues and to determine whether the mitochondrial dysfunction of PBMCs could serve as diagnostic, severity, and/or prognosis biomarkers. Similarly, whether modulating the mitochondrial function of PBMCs improves patient symptoms is still under debate.

This Special Issue will publish original experimental and clinical research data together with literature reviews to investigate the molecular, cellular, and systemic mechanisms by which the mitochondrial function of PBMCs might modulate cardiovascular, respiratory, and muscle functions, both normally and during disease. Data obtained during sepsis or COVID-19 infection are also welcome since PBMC alterations might reduce the efficacy of the immune response when fighting against such bacterial or viral aggressions.

Dr. Bernard Geny
Dr. Marianne Riou
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.

Published Papers (5 papers)

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18 pages, 10788 KiB  
Article
Mitochondrial Oxidative Stress and Mitophagy Activation Contribute to TNF-Dependent Impairment of Myogenesis
by Daniil A. Chernyavskij, Olga Yu. Pletjushkina, Anastasia V. Kashtanova, Ivan I. Galkin, Anna Karpukhina, Boris V. Chernyak, Yegor S. Vassetzky and Ekaterina N. Popova
Antioxidants 2023, 12(3), 602; https://doi.org/10.3390/antiox12030602 - 1 Mar 2023
Cited by 5 | Viewed by 3681
Abstract
Many muscular pathologies are associated with oxidative stress and elevated levels of the tumor necrosis factor (TNF) that cause muscle protein catabolism and impair myogenesis. Myogenesis defects caused by TNF are mediated in part by reactive oxygen species (ROS), including those produced by [...] Read more.
Many muscular pathologies are associated with oxidative stress and elevated levels of the tumor necrosis factor (TNF) that cause muscle protein catabolism and impair myogenesis. Myogenesis defects caused by TNF are mediated in part by reactive oxygen species (ROS), including those produced by mitochondria (mitoROS), but the mechanism of their pathological action is not fully understood. We hypothesized that mitoROS act by triggering and enhancing mitophagy, an important tool for remodelling the mitochondrial reticulum during myogenesis. We used three recently developed probes—MitoTracker Orange CM-H2TMRos, mito-QC, and MitoCLox—to study myogenesis in human myoblasts. Induction of myogenesis resulted in a significant increase in mitoROS generation and phospholipid peroxidation in the inner mitochondrial membrane, as well as mitophagy enhancement. Treatment of myoblasts with TNF 24 h before induction of myogenesis resulted in a significant decrease in the myoblast fusion index and myosin heavy chain (MYH2) synthesis. TNF increased the levels of mitoROS, phospholipid peroxidation in the inner mitochondrial membrane and mitophagy at an early stage of differentiation. Trolox and SkQ1 antioxidants partially restored TNF-impaired myogenesis. The general autophagy inducers rapamycin and AICAR, which also stimulate mitophagy, completely blocked myogenesis. The autophagy suppression by the ULK1 inhibitor SBI-0206965 partially restored myogenesis impaired by TNF. Thus, suppression of myogenesis by TNF is associated with a mitoROS-dependent increase in general autophagy and mitophagy. Full article
(This article belongs to the Special Issue Mitochondrial Functions and Oxidative Stress during Cardiorespiratory and Muscular Diseases)
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Review

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20 pages, 1034 KiB  
Review
Status of Mitochondrial Oxidative Phosphorylation during the Development of Heart Failure
by Sukhwinder K. Bhullar and Naranjan S. Dhalla
Antioxidants 2023, 12(11), 1941; https://doi.org/10.3390/antiox12111941 - 31 Oct 2023
Cited by 6 | Viewed by 1764
Abstract
Mitochondria are specialized organelles, which serve as the “Power House” to generate energy for maintaining heart function. These organelles contain various enzymes for the oxidation of different substrates as well as the electron transport chain in the form of Complexes I to V [...] Read more.
Mitochondria are specialized organelles, which serve as the “Power House” to generate energy for maintaining heart function. These organelles contain various enzymes for the oxidation of different substrates as well as the electron transport chain in the form of Complexes I to V for producing ATP through the process of oxidative phosphorylation (OXPHOS). Several studies have shown depressed OXPHOS activity due to defects in one or more components of the substrate oxidation and electron transport systems which leads to the depletion of myocardial high-energy phosphates (both creatine phosphate and ATP). Such changes in the mitochondria appear to be due to the development of oxidative stress, inflammation, and Ca2+-handling abnormalities in the failing heart. Although some investigations have failed to detect any changes in the OXPHOS activity in the failing heart, such results appear to be due to a loss of Ca2+ during the mitochondrial isolation procedure. There is ample evidence to suggest that mitochondrial Ca2+-overload occurs, which is associated with impaired mitochondrial OXPHOS activity in the failing heart. The depression in mitochondrial OXPHOS activity may also be due to the increased level of reactive oxygen species, which are formed as a consequence of defects in the electron transport complexes in the failing heart. Various metabolic interventions which promote the generation of ATP have been reported to be beneficial for the therapy of heart failure. Accordingly, it is suggested that depression in mitochondrial OXPHOS activity plays an important role in the development of heart failure. Full article
(This article belongs to the Special Issue Mitochondrial Functions and Oxidative Stress during Cardiorespiratory and Muscular Diseases)
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25 pages, 2952 KiB  
Review
Microalgae Produce Antioxidant Molecules with Potential Preventive Effects on Mitochondrial Functions and Skeletal Muscular Oxidative Stress
by Jordi Vignaud, Céline Loiseau, Josiane Hérault, Claire Mayer, Martine Côme, Isabelle Martin and Lionel Ulmann
Antioxidants 2023, 12(5), 1050; https://doi.org/10.3390/antiox12051050 - 5 May 2023
Cited by 7 | Viewed by 4492
Abstract
In recent years, microalgae have become a source of molecules for a healthy life. Their composition of carbohydrates, peptides, lipids, vitamins and carotenoids makes them a promising new source of antioxidant molecules. Skeletal muscle is a tissue that requires constant remodeling via protein [...] Read more.
In recent years, microalgae have become a source of molecules for a healthy life. Their composition of carbohydrates, peptides, lipids, vitamins and carotenoids makes them a promising new source of antioxidant molecules. Skeletal muscle is a tissue that requires constant remodeling via protein turnover, and its regular functioning consumes energy in the form of adenosine triphosphate (ATP), which is produced by mitochondria. Under conditions of traumatic exercise or muscular diseases, a high production of reactive oxygen species (ROS) at the origin of oxidative stress (OS) will lead to inflammation and muscle atrophy, with life-long consequences. In this review, we describe the potential antioxidant effects of microalgae and their biomolecules on mitochondrial functions and skeletal muscular oxidative stress during exercises or in musculoskeletal diseases, as in sarcopenia, chronic obstructive pulmonary disease (COPD) and Duchenne muscular dystrophy (DMD), through the increase in and regulation of antioxidant pathways and protein synthesis. Full article
(This article belongs to the Special Issue Mitochondrial Functions and Oxidative Stress during Cardiorespiratory and Muscular Diseases)
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21 pages, 1242 KiB  
Review
The Role of Lonp1 on Mitochondrial Functions during Cardiovascular and Muscular Diseases
by Giada Zanini, Valentina Selleri, Mara Malerba, Kateryna Solodka, Giorgia Sinigaglia, Milena Nasi, Anna Vittoria Mattioli and Marcello Pinti
Antioxidants 2023, 12(3), 598; https://doi.org/10.3390/antiox12030598 - 28 Feb 2023
Cited by 7 | Viewed by 2997
Abstract
The mitochondrial protease Lonp1 is a multifunctional enzyme that regulates crucial mitochondrial functions, including the degradation of oxidized proteins, folding of imported proteins and maintenance the correct number of copies of mitochondrial DNA. A series of recent studies has put Lonp1 at the [...] Read more.
The mitochondrial protease Lonp1 is a multifunctional enzyme that regulates crucial mitochondrial functions, including the degradation of oxidized proteins, folding of imported proteins and maintenance the correct number of copies of mitochondrial DNA. A series of recent studies has put Lonp1 at the center of the stage in the homeostasis of cardiomyocytes and muscle skeletal cells. During heart development, Lonp1 allows the metabolic shift from anaerobic glycolysis to mitochondrial oxidative phosphorylation. Knock out of Lonp1 arrests heart development and determines cardiomyocyte apoptosis. In adults, Lonp1 acts as a cardioprotective protein, as its upregulation mitigates cardiac injury by preventing the oxidative damage of proteins and lipids, and by preserving mitochondrial redox balance. In skeletal muscle, Lonp1 is crucial for cell development, as it mediates the activation of PINK1/Parkin pathway needed for proper myoblast differentiation. Skeletal muscle-specific ablation of Lonp1 in mice causes reduced muscle fiber size and strength due to the accumulation of mitochondrial-retained protein in muscle. Lonp1 expression and activity decline with age in different tissues, including skeletal muscle, and are associated with a functional decline and structural impairment of muscle fibers. Aerobic exercise increases unfolded protein response markers including Lonp1 in the skeletal muscle of aged animals and is associated with muscle functional recovery. Finally, mutations of Lonp1 cause a syndrome named CODAS (Cerebral, Ocular, Dental, Auricular, and Skeletal anomalies) characterized by the impaired development of multiple organs and tissues, including myocytes. CODAS patients show hypotonia and ptosis, indicative of skeletal muscle reduced performance. Overall, this body of observations points Lonp1 as a crucial regulator of mitochondrial functions in the heart and in skeletal muscle. Full article
(This article belongs to the Special Issue Mitochondrial Functions and Oxidative Stress during Cardiorespiratory and Muscular Diseases)
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13 pages, 1012 KiB  
Review
Mitochondrial Dysfunction in Pulmonary Hypertension
by Gusty Rizky Teguh Ryanto, Ratoe Suraya and Tatsuya Nagano
Antioxidants 2023, 12(2), 372; https://doi.org/10.3390/antiox12020372 - 3 Feb 2023
Cited by 5 | Viewed by 1753
Abstract
Pulmonary hypertension (PH) is a multi-etiological condition with a similar hemodynamic clinical sign and end result of right heart failure. Although its causes vary, a similar link across all the classifications is the presence of mitochondrial dysfunction. Mitochondria, as the powerhouse of the [...] Read more.
Pulmonary hypertension (PH) is a multi-etiological condition with a similar hemodynamic clinical sign and end result of right heart failure. Although its causes vary, a similar link across all the classifications is the presence of mitochondrial dysfunction. Mitochondria, as the powerhouse of the cells, hold a number of vital roles in maintaining normal cellular homeostasis, including the pulmonary vascular cells. As such, any disturbance in the normal functions of mitochondria could lead to major pathological consequences. The Warburg effect has been established as a major finding in PH conditions, but other mitochondria-related metabolic and oxidative stress factors have also been reported, making important contributions to the progression of pulmonary vascular remodeling that is commonly found in PH pathophysiology. In this review, we will discuss the role of the mitochondria in maintaining a normal vasculature, how it could be altered during pulmonary vascular remodeling, and the therapeutic options available that can treat its dysfunction. Full article
(This article belongs to the Special Issue Mitochondrial Functions and Oxidative Stress during Cardiorespiratory and Muscular Diseases)
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