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Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases

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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 (10 May 2023) | Viewed by 98523

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Special Issue Editors

Dr. Gina Cavaliere

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Guest Editor

Department of Pharmaceutical Sciences, University of Perugia, 06126 Perugia, Italy
Interests: metabolic diseases; nutrition; obesity; mitochondrial function; reactive oxygen species; oxidative metabolism
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Maria Pina Mollica

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Guest Editor

Department of Biology, University of Naples Federico II, 80126 Naples, Italy
Interests: oxidative metabolism; nutrition; obesity; metaflammation; mitochondrial function; aging; insulin resistance
Special Issues, Collections and Topics in MDPI journals

Dr. Giovanna Trinchese

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Guest Editor

Department of Biology, University of Naples Federico II, 80126 Naples, Italy
Interests: nutrition; metabolic efficiency; obesity; inflammation; mitochondrial function; oxidative stress; diet-induced disorders; neuroinflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are organelles involved in important and fundamental cellular processes, including energy production through the oxidative phosphorylation system and in various critical signaling pathways. Mitochondria are not static entities but dynamic units that undergo fission and fusion cycles to maintain their structural integrity. They are also the principal site of cellular reactive oxygen species (ROS) production, and an imbalance between the production of ROS and cellular antioxidant defenses leads to alterations to mitochondria integrity. It is well known that impaired mitochondrial integrity is associated with the pathogenesis of various metabolic diseases, non-communicable diseases characterized by inflammatory processes closely related to mitochondrial functions. In recent decades, these organelles have been considered a target of potential therapeutic approaches for the treatment of various diseases. Moreover, molecules naturally produced by plants and a variety of synthetic compounds are capable of modulating mitochondrial function. This Special Issue aims to collect original research and review articles describing the role of mitochondria in metabolic alterations and the potential therapeutic approaches adopted for improving the impaired functionality of mitochondria. Manuscripts that investigate the influence of the natural or chemical compounds that modulate mitochondrial function and the underlying mechanisms will be considered. This data collection can help redefine preventive and therapeutic strategies in an attempt to prevent and counter the onset of metabolic diseases.

Dr. Gina Cavaliere
Prof. Dr. Maria Pina Mollica
Dr. Giovanna Trinchese
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

mitochondria function
oxidative processes
metabolic diseases
reactive oxygen species
therapeutic approaches
mitochondrial integrity
energy production
mitochondrial bioenergetic
metabolism
mitochondrial dynamic

Published Papers (5 papers)

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Research

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25 pages, 3039 KiB

Open AccessArticle

Different Effects of SSRIs, Bupropion, and Trazodone on Mitochondrial Functions and Monoamine Oxidase Isoform Activity

by Matej Ľupták, Zdeněk Fišar and Jana Hroudová

Antioxidants 2023, 12(6), 1208; https://doi.org/10.3390/antiox12061208 - 2 Jun 2023

Cited by 3 | Viewed by 3139

Abstract

Mitochondrial dysfunction is involved in the pathophysiology of psychiatric and neurodegenerative disorders and can be used as a modulator and/or predictor of treatment responsiveness. Understanding the mitochondrial effects of antidepressants is important to connect mitochondria with their therapeutic and/or adverse effects. Pig brain-isolated mitochondria were used to evaluate antidepressant-induced changes in the activity of electron transport chain (ETC) complexes, monoamine oxidase (MAO), mitochondrial respiratory rate, and ATP. Bupropion, escitalopram, fluvoxamine, sertraline, paroxetine, and trazodone were tested. All tested antidepressants showed significant inhibition of complex I and IV activities at high concentrations (50 and 100 µmol/L); complex II + III activity was reduced by all antidepressants except bupropion. Complex I-linked respiration was reduced by escitalopram >> trazodone >> sertraline. Complex II-linked respiration was reduced only by bupropion. Significant positive correlations were confirmed between complex I-linked respiration and the activities of individual ETC complexes. MAO activity was inhibited by all tested antidepressants, with SSRIs causing a greater effect than trazodone and bupropion. The results indicate a probable association between the adverse effects of high doses of antidepressants and drug-induced changes in the activity of ETC complexes and the respiratory rate of mitochondria. In contrast, MAO inhibition could be linked to the antidepressant, procognitive, and neuroprotective effects of the tested antidepressants. Full article

(This article belongs to the Special Issue Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases)

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Review

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23 pages, 821 KiB

Open AccessReview

From Obesity-Induced Low-Grade Inflammation to Lipotoxicity and Mitochondrial Dysfunction: Altered Multi-Crosstalk between Adipose Tissue and Metabolically Active Organs

by Gina Cavaliere, Fabiano Cimmino, Giovanna Trinchese, Angela Catapano, Lidia Petrella, Margherita D’Angelo, Lucio Lucchin and Maria Pina Mollica

Antioxidants 2023, 12(6), 1172; https://doi.org/10.3390/antiox12061172 - 29 May 2023

Cited by 8 | Viewed by 3665

Abstract

Obesity is a major risk factor for several metabolic diseases, including type 2 diabetes, hyperlipidemia, cardiovascular diseases, and brain disorders. Growing evidence suggests the importance of inter-organ metabolic communication for the progression of obesity and the subsequent onset of related disorders. This review provides a broad overview of the pathophysiological processes that from adipose tissue dysfunction leading to altered multi-tissue crosstalk relevant to regulating energy homeostasis and the etiology of obesity. First, a comprehensive description of the role of adipose tissue was reported. Then, attention was turned toward the unhealthy expansion of adipose tissue, low-grade inflammatory state, metabolic inflexibility, and mitochondrial dysfunction as root causes of systemic metabolic alterations. In addition, a short spot was devoted to iron deficiency in obese conditions and the role of the hepcidin–ferroportin relationship in the management of this issue. Finally, different classes of bioactive food components were described with a perspective to enhance their potential preventive and therapeutic use against obesity-related diseases. Full article

(This article belongs to the Special Issue Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases)

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22 pages, 2135 KiB

Open AccessReview

Mitochondrial Fission as a Therapeutic Target for Metabolic Diseases: Insights into Antioxidant Strategies

by Tianzheng Yu, Li Wang, Lei Zhang and Patricia A. Deuster

Antioxidants 2023, 12(6), 1163; https://doi.org/10.3390/antiox12061163 - 27 May 2023

Cited by 9 | Viewed by 2617

Abstract

Mitochondrial fission is a crucial process in maintaining metabolic homeostasis in normal physiology and under conditions of stress. Its dysregulation has been associated with several metabolic diseases, including, but not limited to, obesity, type 2 diabetes (T2DM), and cardiovascular diseases. Reactive oxygen species (ROS) serve a vital role in the genesis of these conditions, and mitochondria are both the main sites of ROS production and the primary targets of ROS. In this review, we explore the physiological and pathological roles of mitochondrial fission, its regulation by dynamin-related protein 1 (Drp1), and the interplay between ROS and mitochondria in health and metabolic diseases. We also discuss the potential therapeutic strategies of targeting mitochondrial fission through antioxidant treatments for ROS-induced conditions, including the effects of lifestyle interventions, dietary supplements, and chemicals, such as mitochondrial division inhibitor-1 (Mdivi-1) and other mitochondrial fission inhibitors, as well as certain commonly used drugs for metabolic diseases. This review highlights the importance of understanding the role of mitochondrial fission in health and metabolic diseases, and the potential of targeting mitochondrial fission as a therapeutic approach to protecting against these conditions. Full article

(This article belongs to the Special Issue Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases)

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24 pages, 2825 KiB

Open AccessReview

PGC-1α Is a Master Regulator of Mitochondrial Lifecycle and ROS Stress Response

by Othman Abu Shelbayeh, Tasnim Arroum, Silke Morris and Karin B. Busch

Antioxidants 2023, 12(5), 1075; https://doi.org/10.3390/antiox12051075 - 10 May 2023

Cited by 33 | Viewed by 6028

Abstract

Mitochondria play a major role in ROS production and defense during their life cycle. The transcriptional activator PGC-1α is a key player in the homeostasis of energy metabolism and is therefore closely linked to mitochondrial function. PGC-1α responds to environmental and intracellular conditions and is regulated by SIRT1/3, TFAM, and AMPK, which are also important regulators of mitochondrial biogenesis and function. In this review, we highlight the functions and regulatory mechanisms of PGC-1α within this framework, with a focus on its involvement in the mitochondrial lifecycle and ROS metabolism. As an example, we show the role of PGC-1α in ROS scavenging under inflammatory conditions. Interestingly, PGC-1α and the stress response factor NF-κB, which regulates the immune response, are reciprocally regulated. During inflammation, NF-κB reduces PGC-1α expression and activity. Low PGC-1α activity leads to the downregulation of antioxidant target genes resulting in oxidative stress. Additionally, low PGC-1α levels and concomitant oxidative stress promote NF-κB activity, which exacerbates the inflammatory response. Full article

(This article belongs to the Special Issue Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases)

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30 pages, 3264 KiB

Open AccessReview

The Key Role of Mitochondrial Function in Health and Disease

by Iñigo San-Millán

Antioxidants 2023, 12(4), 782; https://doi.org/10.3390/antiox12040782 - 23 Mar 2023

Cited by 32 | Viewed by 81902

Abstract

The role of mitochondrial function in health and disease has become increasingly recognized, particularly in the last two decades. Mitochondrial dysfunction as well as disruptions of cellular bioenergetics have been shown to be ubiquitous in some of the most prevalent diseases in our society, such as type 2 diabetes, cardiovascular disease, metabolic syndrome, cancer, and Alzheimer’s disease. However, the etiology and pathogenesis of mitochondrial dysfunction in multiple diseases have yet to be elucidated, making it one of the most significant medical challenges in our history. However, the rapid advances in our knowledge of cellular metabolism coupled with the novel understanding at the molecular and genetic levels show tremendous promise to one day elucidate the mysteries of this ancient organelle in order to treat it therapeutically when needed. Mitochondrial DNA mutations, infections, aging, and a lack of physical activity have been identified to be major players in mitochondrial dysfunction in multiple diseases. This review examines the complexities of mitochondrial function, whose ancient incorporation into eukaryotic cells for energy purposes was key for the survival and creation of new species. Among these complexities, the tightly intertwined bioenergetics derived from the combustion of alimentary substrates and oxygen are necessary for cellular homeostasis, including the production of reactive oxygen species. This review discusses different etiological mechanisms by which mitochondria could become dysregulated, determining the fate of multiple tissues and organs and being a protagonist in the pathogenesis of many non–communicable diseases. Finally, physical activity is a canonical evolutionary characteristic of humans that remains embedded in our genes. The normalization of a lack of physical activity in our modern society has led to the perception that exercise is an “intervention”. However, physical activity remains the modus vivendi engrained in our genes and being sedentary has been the real intervention and collateral effect of modern societies. It is well known that a lack of physical activity leads to mitochondrial dysfunction and, hence, it probably becomes a major etiological factor of many non–communicable diseases affecting modern societies. Since physical activity remains the only stimulus we know that can improve and maintain mitochondrial function, a significant emphasis on exercise promotion should be imperative in order to prevent multiple diseases. Finally, in populations with chronic diseases where mitochondrial dysfunction is involved, an individualized exercise prescription should be crucial for the “metabolic rehabilitation” of many patients. From lessons learned from elite athletes (the perfect human machines), it is possible to translate and apply multiple concepts to the betterment of populations with chronic diseases. Full article

(This article belongs to the Special Issue Oxidative Metabolism and Mitochondrial Dysfunction in Metabolic Diseases)

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