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Antioxidants
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The Versatility of Mitochondrial Calcium: Insights in the Regulation of...
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The Versatility of Mitochondrial Calcium: Insights in the Regulation of Redox Signaling

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

Deadline for manuscript submissions: closed (15 September 2023) | Viewed by 10557

Special Issue Editor

Dr. Giampaolo Morciano

E-Mail Website
Guest Editor
Laboratory for Technologies of Advanced Therapies, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy
Interests: mitochondria; cardiovascular diseases; cell signaling; hypoxia; mitochondrial diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

This Special Issue will highlight studies relating to the interplay between calcium and redox signaling. Calcium (Ca2+) is a crucial second messenger involved in intracellular molecular routes, and it plays an essential role in cell fate decisions from birth, through to development, and finally to death. Ca2+ signaling is put in place by an intricate network of proteins, differently localized inside cells which sense and spread Ca2+ signals by spatio-temporal means in order to regulate cellular processes. Ca2+ signaling pathways interact with other cellular signaling systems such as reactive oxygen species (ROS). Originally considered as simple detrimental by-products of metabolism, it is now evident that ROS generated in sub-toxic amounts may act as signaling molecules involved in various physio-pathological processes. This Special Issue aims to collect papers (both original articles and review) which highlight the crosstalk of these two systems in physiology, and how this can be dysregulated in human diseases generating potentially harmful effects.

Dr. Giampaolo Morciano
Guest Editor

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

  • mitochondria
  • calcium signaling
  • ROS
  • diseases
  • cell signaling

Published Papers (4 papers)

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Research

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15 pages, 2976 KiB  
Article
Cerium-Doped Self-Assembling Nanoparticles as a Novel Anti-Oxidant Delivery System Preserving Mitochondrial Function in Cortical Neurons Exposed to Ischemia-like Conditions
by Valeria Nele, Valentina Tedeschi, Virginia Campani, Raffaella Ciancio, Alessia Angelillo, Sossio Fabio Graziano, Giuseppe De Rosa and Agnese Secondo
Antioxidants 2023, 12(2), 358; https://doi.org/10.3390/antiox12020358 - 02 Feb 2023
Cited by 4 | Viewed by 1439
Abstract
Neurodegenerative diseases are characterized by mitochondrial dysfunction leading to abnormal levels of reactive oxygen species (ROS), making the use of ROS-scavenging nanomaterials a promising therapeutic approach. Here, we combined the unique ROS-scavenging properties of cerium-based nanomaterials with the lipid self-assembling nanoparticles (SANP) technology. [...] Read more.
Neurodegenerative diseases are characterized by mitochondrial dysfunction leading to abnormal levels of reactive oxygen species (ROS), making the use of ROS-scavenging nanomaterials a promising therapeutic approach. Here, we combined the unique ROS-scavenging properties of cerium-based nanomaterials with the lipid self-assembling nanoparticles (SANP) technology. We optimized the preparation of cerium-doped SANP (Ce-SANP) and characterized the formulations in terms of both physiochemical and biological properties. Ce-SANP exhibited good colloidal properties and were able to mimic the activity of two ROS-scavenging enzymes, namely peroxidase and super oxide dismutase. Under ischemia-like conditions, Ce-SANP could rescue neuronal cells from mitochondrial suffering by reducing ROS production and preventing ATP level reduction. Furthermore, Ce-SANP prevented mitochondrial Ca2+ homeostasis dysfunction, partially restoring mitochondrial Ca2+ handling. Taken together, these results highlight the potential of the anti-oxidant Ce-SANP platform technology to manage ROS levels and mitochondrial function for the treatment of neurodegenerative diseases. Full article
(This article belongs to the Special Issue The Versatility of Mitochondrial Calcium: Insights in the Regulation of Redox Signaling)
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Review

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29 pages, 4037 KiB  
Review
Therapeutic Potential of Heterocyclic Compounds Targeting Mitochondrial Calcium Homeostasis and Signaling in Alzheimer’s Disease and Parkinson’s Disease
by Victor Tapias, Paula González-Andrés, Laura F. Peña, Asunción Barbero, Lucía Núñez and Carlos Villalobos
Antioxidants 2023, 12(6), 1282; https://doi.org/10.3390/antiox12061282 - 15 Jun 2023
Cited by 2 | Viewed by 1806
Abstract
Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative diseases in the elderly. The key histopathological features of these diseases are the presence of abnormal protein aggregates and the progressive and irreversible loss of neurons in specific brain regions. [...] Read more.
Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative diseases in the elderly. The key histopathological features of these diseases are the presence of abnormal protein aggregates and the progressive and irreversible loss of neurons in specific brain regions. The exact mechanisms underlying the etiopathogenesis of AD or PD remain unknown, but there is extensive evidence indicating that excessive generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), along with a depleted antioxidant system, mitochondrial dysfunction, and intracellular Ca2+ dyshomeostasis, plays a vital role in the pathophysiology of these neurological disorders. Due to an improvement in life expectancy, the incidence of age-related neurodegenerative diseases has significantly increased. However, there is no effective protective treatment or therapy available but rather only very limited palliative treatment. Therefore, there is an urgent need for the development of preventive strategies and disease-modifying therapies to treat AD/PD. Because dysregulated Ca2+ metabolism drives oxidative damage and neuropathology in these diseases, the identification or development of compounds capable of restoring Ca2+ homeostasis and signaling may provide a neuroprotective avenue for the treatment of neurodegenerative diseases. In addition, a set of strategies to control mitochondrial Ca2+ homeostasis and signaling has been reported, including decreased Ca2+ uptake through voltage-operated Ca2+ channels (VOCCs). In this article, we review the modulatory effects of several heterocyclic compounds on Ca2+ homeostasis and trafficking, as well as their ability to regulate compromised mitochondrial function and associated free-radical production during the onset and progression of AD or PD. This comprehensive review also describes the chemical synthesis of the heterocycles and summarizes the clinical trial outcomes. Full article
(This article belongs to the Special Issue The Versatility of Mitochondrial Calcium: Insights in the Regulation of Redox Signaling)
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19 pages, 696 KiB  
Review
Calcium and Reactive Oxygen Species Signaling Interplays in Cardiac Physiology and Pathologies
by Bianca De Nicolo, Erica Cataldi-Stagetti, Chiara Diquigiovanni and Elena Bonora
Antioxidants 2023, 12(2), 353; https://doi.org/10.3390/antiox12020353 - 02 Feb 2023
Cited by 10 | Viewed by 3563
Abstract
Mitochondria are key players in energy production, critical activity for the smooth functioning of energy-demanding organs such as the muscles, brain, and heart. Therefore, dysregulation or alterations in mitochondrial bioenergetics primarily perturb these organs. Within the cell, mitochondria are the major site of [...] Read more.
Mitochondria are key players in energy production, critical activity for the smooth functioning of energy-demanding organs such as the muscles, brain, and heart. Therefore, dysregulation or alterations in mitochondrial bioenergetics primarily perturb these organs. Within the cell, mitochondria are the major site of reactive oxygen species (ROS) production through the activity of different enzymes since it is one of the organelles with the major availability of oxygen. ROS can act as signaling molecules in a number of different pathways by modulating calcium (Ca2+) signaling. Interactions among ROS and calcium signaling can be considered bidirectional, with ROS regulating cellular Ca2+ signaling, whereas Ca2+ signaling is essential for ROS production. In particular, we will discuss how alterations in the crosstalk between ROS and Ca2+ can lead to mitochondrial bioenergetics dysfunctions and the consequent damage to tissues at high energy demand, such as the heart. Changes in Ca2+ can induce mitochondrial alterations associated with reduced ATP production and increased production of ROS. These changes in Ca2+ levels and ROS generation completely paralyze cardiac contractility. Thus, ROS can hinder the excitation–contraction coupling, inducing arrhythmias, hypertrophy, apoptosis, or necrosis of cardiac cells. These interplays in the cardiovascular system are the focus of this review. Full article
(This article belongs to the Special Issue The Versatility of Mitochondrial Calcium: Insights in the Regulation of Redox Signaling)
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Other

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45 pages, 1737 KiB  
Systematic Review
Schizophrenia Synaptic Pathology and Antipsychotic Treatment in the Framework of Oxidative and Mitochondrial Dysfunction: Translational Highlights for the Clinics and Treatment
by Giuseppe De Simone, Benedetta Mazza, Licia Vellucci, Annarita Barone, Mariateresa Ciccarelli and Andrea de Bartolomeis
Antioxidants 2023, 12(4), 975; https://doi.org/10.3390/antiox12040975 - 21 Apr 2023
Cited by 5 | Viewed by 3092
Abstract
Schizophrenia is a worldwide mental illness characterized by alterations at dopaminergic and glutamatergic synapses resulting in global dysconnectivity within and between brain networks. Impairments in inflammatory processes, mitochondrial functions, energy expenditure, and oxidative stress have been extensively associated with schizophrenia pathophysiology. Antipsychotics, the [...] Read more.
Schizophrenia is a worldwide mental illness characterized by alterations at dopaminergic and glutamatergic synapses resulting in global dysconnectivity within and between brain networks. Impairments in inflammatory processes, mitochondrial functions, energy expenditure, and oxidative stress have been extensively associated with schizophrenia pathophysiology. Antipsychotics, the mainstay of schizophrenia pharmacological treatment and all sharing the common feature of dopamine D2 receptor occupancy, may affect antioxidant pathways as well as mitochondrial protein levels and gene expression. Here, we systematically reviewed the available evidence on antioxidants’ mechanisms in antipsychotic action and the impact of first- and second-generation compounds on mitochondrial functions and oxidative stress. We further focused on clinical trials addressing the efficacy and tolerability of antioxidants as an augmentation strategy of antipsychotic treatment. EMBASE, Scopus, and Medline/PubMed databases were interrogated. The selection process was conducted in respect of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) criteria. Several mitochondrial proteins involved in cell viability, energy metabolism, and regulation of oxidative systems were reported to be significantly modified by antipsychotic treatment with differences between first- and second-generation drugs. Finally, antioxidants may affect cognitive and psychotic symptoms in patients with schizophrenia, and although the evidence is only preliminary, the results indicate that further studies are warranted. Full article
(This article belongs to the Special Issue The Versatility of Mitochondrial Calcium: Insights in the Regulation of Redox Signaling)
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