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Antioxidants
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Mitochondrial Oxidative and Nitrosative Stress as a Therapeutic Target in...
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Mitochondrial Oxidative and Nitrosative Stress as a Therapeutic Target in Diseases

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (31 July 2020) | Viewed by 53213

Special Issue Editors

Dr. Anna Colell

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Guest Editor
Department of Cell Death and Proliferation, Institut D'Investigacions Biomèdiques de Barcelona, Consejo Superior de Investigaciones Científicas (IIBB-CSIC), Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), 08036 Barcelona, Spain
Interests: Alzheimer’s disease; cholesterol in neurodegeneration; mitochondria; mitochondrial oxidative stress; autophagy/mitophagy
Special Issues, Collections and Topics in MDPI journals
Dr. Montserrat Marí

E-Mail Website
Guest Editor
Department of Cell Death and Proliferation, Institut D'Investigacions Biomèdiques de Barcelona, Consejo Superior de Investigaciones Científicas (IIBB-CSIC), Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), 08036 Barcelona, Spain
Interests: liver diseases; nafld; liver fibrosis; nkt cells; liver immunology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Although necessary for life, mitochondria are often essential for initiating apoptotic death and deciding cell fate under cellular stress. Recently, in addition to their role in cell death, mitochondria have been suggested to serve as signaling platforms critical for regulating autophagy and the inflammatory response. Mitochondrial oxidative/nitrosative stress has been reported to trigger autophagy by promoting autophagosome formation and induce the release of inflammatory cytokines through the activation of the NLRP3-inflammasome. Thus, it is becoming clear that mitochondria participate in many aspects of cell function, and evidence further suggests that mitochondria impairment is underlying many common human disorders. Consequently, new strategies are being sought to restore the mitochondrial function therapeutically.

Contributions to this Special Issue may cover research findings or review articles related to the role of mitochondrial oxidative stress and mitochondrial dysfunction in different pathological conditions ranging from cancer to neurodegenerative diseases, the mechanistic links between changes in mitochondria functionality and alterations of cellular processes such as autophagy and the inflammatory signaling pathways and its impact on cell viability, and the use of mitochondria-targeted molecules, including antioxidants, as therapeutic strategies for disease intervention.

Dr. Anna Colell
Dr. Montserrat Marí
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

  • Mitochondrial oxidative stress
  • Autophagy
  • mitophagy
  • Inflammasome
  • Antioxidants
  • Mitochondrial dysfunction
  • Mitochondrial-targeted molecules
  • Disease

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Related Special Issues

Published Papers (8 papers)

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Editorial

Jump to: Research, Review

2 pages, 185 KiB  
Editorial
Mitochondrial Oxidative and Nitrosative Stress as a Therapeutic Target in Diseases
by Montserrat Marí and Anna Colell
Antioxidants 2021, 10(2), 314; https://doi.org/10.3390/antiox10020314 - 20 Feb 2021
Cited by 9 | Viewed by 1789
Abstract
Mitochondria are fundamental to life [...] Full article
(This article belongs to the Special Issue Mitochondrial Oxidative and Nitrosative Stress as a Therapeutic Target in Diseases)

Research

Jump to: Editorial, Review

22 pages, 4798 KiB  
Article
Post-Translational Modification Analysis of VDAC1 in ALS-SOD1 Model Cells Reveals Specific Asparagine and Glutamine Deamidation
by Maria Gaetana Giovanna Pittalà, Simona Reina, Salvatore Antonio Maria Cubisino, Annamaria Cucina, Beatrice Formicola, Vincenzo Cunsolo, Salvatore Foti, Rosaria Saletti and Angela Messina
Antioxidants 2020, 9(12), 1218; https://doi.org/10.3390/antiox9121218 - 2 Dec 2020
Cited by 13 | Viewed by 3379
Abstract
Mitochondria from affected tissues of amyotrophic lateral sclerosis (ALS) patients show morphological and biochemical abnormalities. Mitochondrial dysfunction causes oxidative damage and the accumulation of ROS, and represents one of the major triggers of selective death of motor neurons in ALS. We aimed to [...] Read more.
Mitochondria from affected tissues of amyotrophic lateral sclerosis (ALS) patients show morphological and biochemical abnormalities. Mitochondrial dysfunction causes oxidative damage and the accumulation of ROS, and represents one of the major triggers of selective death of motor neurons in ALS. We aimed to assess whether oxidative stress in ALS induces post-translational modifications (PTMs) in VDAC1, the main protein of the outer mitochondrial membrane and known to interact with SOD1 mutants related to ALS. In this work, specific PTMs of the VDAC1 protein purified by hydroxyapatite from mitochondria of a NSC34 cell line expressing human SOD1G93A, a suitable ALS motor neuron model, were analyzed by tryptic and chymotryptic proteolysis and UHPLC/High-Resolution ESI-MS/MS. We found selective deamidations of asparagine and glutamine of VDAC1 in ALS-related NSC34-SOD1G93A cells but not in NSC34-SOD1WT or NSC34 cells. In addition, we identified differences in the over-oxidation of methionine and cysteines between VDAC1 purified from ALS model or non-ALS NSC34 cells. The specific range of PTMs identified exclusively in VDAC1 from NSC34-SOD1G93A cells but not from NSC34 control lines, suggests the appearance of important changes to the structure of the VDAC1 channel and therefore to the bioenergetics metabolism of ALS motor neurons. Data are available via ProteomeXchange with identifier <PXD022598>. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative and Nitrosative Stress as a Therapeutic Target in Diseases)
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17 pages, 1449 KiB  
Article
Irisin Mitigates Oxidative Stress, Chondrocyte Dysfunction and Osteoarthritis Development through Regulating Mitochondrial Integrity and Autophagy
by Feng-Sheng Wang, Chung-Wen Kuo, Jih-Yang Ko, Yu-Shan Chen, Shao-Yu Wang, Huei-Jing Ke, Pei-Chen Kuo, Chin-Huei Lee, Jian-Ching Wu, Wen-Bin Lu, Ming-Hong Tai, Holger Jahr and Wei-Shiung Lian
Antioxidants 2020, 9(9), 810; https://doi.org/10.3390/antiox9090810 - 1 Sep 2020
Cited by 101 | Viewed by 7370
Abstract
Compromised autophagy and mitochondrial dysfunction downregulate chondrocytic activity, accelerating the development of osteoarthritis (OA). Irisin, a cleaved form of fibronectin type III domain containing 5 (FNDC5), regulates bone turnover and muscle homeostasis. Little is known about the effect of Irisin on chondrocytes and [...] Read more.
Compromised autophagy and mitochondrial dysfunction downregulate chondrocytic activity, accelerating the development of osteoarthritis (OA). Irisin, a cleaved form of fibronectin type III domain containing 5 (FNDC5), regulates bone turnover and muscle homeostasis. Little is known about the effect of Irisin on chondrocytes and the development of osteoarthritis. This study revealed that human osteoarthritic articular chondrocytes express decreased level of FNDC5 and autophagosome marker LC3-II but upregulated levels of oxidative DNA damage marker 8-hydroxydeoxyguanosine (8-OHdG) and apoptosis. Intra-articular administration of Irisin further alleviated symptoms of medial meniscus destabilization, like cartilage erosion and synovitis, while improved the gait profiles of the injured legs. Irisin treatment upregulated autophagy, 8-OHdG and apoptosis in chondrocytes of the injured cartilage. In vitro, Irisin improved IL-1β-mediated growth inhibition, loss of specific cartilage markers and glycosaminoglycan production by chondrocytes. Irisin also reversed Sirt3 and UCP-1 pathways, thereby improving mitochondrial membrane potential, ATP production, and catalase to attenuated IL-1β-mediated reactive oxygen radical production, mitochondrial fusion, mitophagy, and autophagosome formation. Taken together, FNDC5 loss in chondrocytes is correlated with human knee OA. Irisin repressed inflammation-mediated oxidative stress and extracellular matrix underproduction through retaining mitochondrial biogenesis, dynamics and autophagic program. Our analyses shed new light on the chondroprotective actions of this myokine, and highlight the remedial effects of Irisin on OA development. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative and Nitrosative Stress as a Therapeutic Target in Diseases)
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13 pages, 2616 KiB  
Article
Toxicity of Necrostatin-1 in Parkinson’s Disease Models
by Eva Alegre-Cortés, Alicia Muriel-González, Saray Canales-Cortés, Elisabet Uribe-Carretero, Guadalupe Martínez-Chacón, Ana Aiastui, Adolfo López de Munain, Mireia Niso-Santano, Rosa A. Gonzalez-Polo, José M. Fuentes and Sokhna M. S. Yakhine-Diop
Antioxidants 2020, 9(6), 524; https://doi.org/10.3390/antiox9060524 - 15 Jun 2020
Cited by 17 | Viewed by 4699
Abstract
Parkinson’s disease (PD) is a neurodegenerative disorder that is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta. This neuronal loss, inherent to age, is related to exposure to environmental toxins and/or a genetic predisposition. PD-induced cell death has [...] Read more.
Parkinson’s disease (PD) is a neurodegenerative disorder that is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta. This neuronal loss, inherent to age, is related to exposure to environmental toxins and/or a genetic predisposition. PD-induced cell death has been studied thoroughly, but its characterization remains elusive. To date, several types of cell death, including apoptosis, autophagy-induced cell death, and necrosis, have been implicated in PD progression. In this study, we evaluated necroptosis, which is a programmed type of necrosis, in primary fibroblasts from PD patients with and without the G2019S leucine-rich repeat kinase 2 (LRRK2) mutation and in rotenone-treated cells (SH-SY5Y and fibroblasts). The results showed that programmed necrosis was not activated in the cells of PD patients, but it was activated in cells exposed to rotenone. Necrostatin-1 (Nec-1), an inhibitor of the necroptosis pathway, prevented rotenone-induced necroptosis in PD models. However, Nec-1 affected mitochondrial morphology and failed to protect mitochondria against rotenone toxicity. Therefore, despite the inhibition of rotenone-mediated necroptosis, PD models were susceptible to the effects of both Nec-1 and rotenone. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative and Nitrosative Stress as a Therapeutic Target in Diseases)
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Review

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29 pages, 1174 KiB  
Review
The Impact of Mitochondrial Deficiencies in Neuromuscular Diseases
by Judith Cantó-Santos, Josep M. Grau-Junyent and Glòria Garrabou
Antioxidants 2020, 9(10), 964; https://doi.org/10.3390/antiox9100964 - 9 Oct 2020
Cited by 23 | Viewed by 7309
Abstract
Neuromuscular diseases (NMDs) are a heterogeneous group of acquired or inherited rare disorders caused by injury or dysfunction of the anterior horn cells of the spinal cord (lower motor neurons), peripheral nerves, neuromuscular junctions, or skeletal muscles leading to muscle weakness and waste. [...] Read more.
Neuromuscular diseases (NMDs) are a heterogeneous group of acquired or inherited rare disorders caused by injury or dysfunction of the anterior horn cells of the spinal cord (lower motor neurons), peripheral nerves, neuromuscular junctions, or skeletal muscles leading to muscle weakness and waste. Unfortunately, most of them entail serious or even fatal consequences. The prevalence rates among NMDs range between 1 and 10 per 100,000 population, but their rarity and diversity pose difficulties for healthcare and research. Some molecular hallmarks are being explored to elucidate the mechanisms triggering disease, to set the path for further advances. In fact, in the present review we outline the metabolic alterations of NMDs, mainly focusing on the role of mitochondria. The aim of the review is to discuss the mechanisms underlying energy production, oxidative stress generation, cell signaling, autophagy, and inflammation triggered or conditioned by the mitochondria. Briefly, increased levels of inflammation have been linked to reactive oxygen species (ROS) accumulation, which is key in mitochondrial genomic instability and mitochondrial respiratory chain (MRC) dysfunction. ROS burst, impaired autophagy, and increased inflammation are observed in many NMDs. Increasing knowledge of the etiology of NMDs will help to develop better diagnosis and treatments, eventually reducing the health and economic burden of NMDs for patients and healthcare systems. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative and Nitrosative Stress as a Therapeutic Target in Diseases)
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21 pages, 1349 KiB  
Review
Mitochondrial Glutathione: Recent Insights and Role in Disease
by Montserrat Marí, Estefanía de Gregorio, Cristina de Dios, Vicente Roca-Agujetas, Blanca Cucarull, Anna Tutusaus, Albert Morales and Anna Colell
Antioxidants 2020, 9(10), 909; https://doi.org/10.3390/antiox9100909 - 24 Sep 2020
Cited by 112 | Viewed by 15851
Abstract
Mitochondria are the main source of reactive oxygen species (ROS), most of them deriving from the mitochondrial respiratory chain. Among the numerous enzymatic and non-enzymatic antioxidant systems present in mitochondria, mitochondrial glutathione (mGSH) emerges as the main line of defense for maintaining the [...] Read more.
Mitochondria are the main source of reactive oxygen species (ROS), most of them deriving from the mitochondrial respiratory chain. Among the numerous enzymatic and non-enzymatic antioxidant systems present in mitochondria, mitochondrial glutathione (mGSH) emerges as the main line of defense for maintaining the appropriate mitochondrial redox environment. mGSH’s ability to act directly or as a co-factor in reactions catalyzed by other mitochondrial enzymes makes its presence essential to avoid or to repair oxidative modifications that can lead to mitochondrial dysfunction and subsequently to cell death. Since mitochondrial redox disorders play a central part in many diseases, harboring optimal levels of mGSH is vitally important. In this review, we will highlight the participation of mGSH as a contributor to disease progression in pathologies as diverse as Alzheimer’s disease, alcoholic and non-alcoholic steatohepatitis, or diabetic nephropathy. Furthermore, the involvement of mitochondrial ROS in the signaling of new prescribed drugs and in other pathologies (or in other unmet medical needs, such as gender differences or coronavirus disease of 2019 (COVID-19) treatment) is still being revealed; guaranteeing that research on mGSH will be an interesting topic for years to come. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative and Nitrosative Stress as a Therapeutic Target in Diseases)
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Graphical abstract

21 pages, 2642 KiB  
Review
Microbiota-Mitochondria Inter-Talk: A Potential Therapeutic Strategy in Obesity and Type 2 Diabetes
by Teresa Vezza, Zaida Abad-Jiménez, Miguel Marti-Cabrera, Milagros Rocha and Víctor Manuel Víctor
Antioxidants 2020, 9(9), 848; https://doi.org/10.3390/antiox9090848 - 10 Sep 2020
Cited by 32 | Viewed by 6204
Abstract
The rising prevalence of obesity and type 2 diabetes (T2D) is a growing concern worldwide. New discoveries in the field of metagenomics and clinical research have revealed that the gut microbiota plays a key role in these metabolic disorders. The mechanisms regulating microbiota [...] Read more.
The rising prevalence of obesity and type 2 diabetes (T2D) is a growing concern worldwide. New discoveries in the field of metagenomics and clinical research have revealed that the gut microbiota plays a key role in these metabolic disorders. The mechanisms regulating microbiota composition are multifactorial and include resistance to stress, presence of pathogens, diet, cultural habits and general health conditions. Recent evidence has shed light on the influence of microbiota quality and diversity on mitochondrial functions. Of note, the gut microbiota has been shown to regulate crucial transcription factors, coactivators, as well as enzymes implicated in mitochondrial biogenesis and metabolism. Moreover, microbiota metabolites seem to interfere with mitochondrial oxidative/nitrosative stress and autophagosome formation, thus regulating the activation of the inflammasome and the production of inflammatory cytokines, key players in chronic metabolic disorders. This review focuses on the association between intestinal microbiota and mitochondrial function and examines the mechanisms that may be the key to their use as potential therapeutic strategies in obesity and T2D management. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative and Nitrosative Stress as a Therapeutic Target in Diseases)
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22 pages, 1828 KiB  
Review
Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease
by D. Allan Butterfield and Debra Boyd-Kimball
Antioxidants 2020, 9(9), 818; https://doi.org/10.3390/antiox9090818 - 2 Sep 2020
Cited by 50 | Viewed by 5462
Abstract
Oxidative and nitrosative stress are widely recognized as critical factors in the pathogenesis and progression of Alzheimer disease (AD) and its earlier stage, amnestic mild cognitive impairment (MCI). A major source of free radicals that lead to oxidative and nitrosative damage is mitochondria. [...] Read more.
Oxidative and nitrosative stress are widely recognized as critical factors in the pathogenesis and progression of Alzheimer disease (AD) and its earlier stage, amnestic mild cognitive impairment (MCI). A major source of free radicals that lead to oxidative and nitrosative damage is mitochondria. This review paper discusses oxidative and nitrosative stress and markers thereof in the brain, along with redox proteomics, which are techniques that have been pioneered in the Butterfield laboratory. Selected biological alterations in—and oxidative and nitrosative modifications of—mitochondria in AD and MCI and systems of relevance thereof also are presented. The review article concludes with a section on the implications of mitochondrial oxidative and nitrosative stress in MCI and AD with respect to imaging studies in and targeted therapies toward these disorders. Taken together, this review provides support for the notion that brain mitochondrial alterations in AD and MCI are key components of oxidative and nitrosative stress observed in these two disorders, and as such, they provide potentially promising therapeutic targets to slow—and hopefully one day stop—the progression of AD, which is a devastating dementing disorder. Full article
(This article belongs to the Special Issue Mitochondrial Oxidative and Nitrosative Stress as a Therapeutic Target in Diseases)
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