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Biomolecules
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Mitochondrial ROS in Health and Disease
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Mitochondrial ROS in Health and Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 7791

Special Issue Editor

Dr. Frank Krause

E-Mail Website
Guest Editor
Nanolytics Gesellschaft für Kolloidanalytik mbH, 14476 Potsdam, Germany
Interests: proteomics; protein-protein interactions; protein-ligand interactions; oxidative phosphorylation; mitochondria; metabolons; aging research; drug discovery; native electrophoresis; analytical ultracentrifugation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are extremely membrane-rich organelles with a central role in metabolism and key functions in cellular signaling and cell survival as well. Therefore, mitochondria are involved in various diseases and the aging process, which has been providing a major impetus for extensive research on mitochondrial structure and function. In recent decades, many essential physiological roles of (mitochondrial) ROS were (re)established, such as in the immune response, cell cycle, and lifespan control.

Though the detrimental role of free radicals and other reactive species on organisms was the prevailing view for a long time, the health- and lifespan-promoting effects of ROS are an emerging topic with some predominantly forgotten roots, e.g., about the medicinal benefits of hydrogen peroxide dating more than a hundred years back. Similarly, many medicinally powerful biomolecules exert oxidative effects either directly or indirectly, including via mitochondrial ROS generation, e.g., paclitaxel and artemisinin.

This Special Issue focuses on the current advances in mitochondrial-derived ROS and their effects on health and disease involving natural-based biomolecules. Both review manuscripts and original research articles are welcome to convey up-to-date insights and avenues of future research.

Dr. Frank Krause
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. Biomolecules 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 2700 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

  • aging
  • apoptosis
  • respiratory chain
  • redox signaling
  • paclitaxel

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Published Papers (4 papers)

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Research

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19 pages, 2747 KiB  
Article
Pathological Defects in a Drosophila Model of Alzheimer’s Disease and Beneficial Effects of the Natural Product Lisosan G
by Silvia Bongiorni, Elisabetta Catalani, Ivan Arisi, Francesca Lazzarini, Simona Del Quondam, Kashi Brunetti, Davide Cervia and Giorgio Prantera
Biomolecules 2024, 14(7), 855; https://doi.org/10.3390/biom14070855 - 15 Jul 2024
Cited by 1 | Viewed by 1411
Abstract
Alzheimer’s disease (AD) brains are histologically marked by the presence of intracellular and extracellular amyloid deposits, which characterize the onset of the disease pathogenesis. Increasing evidence suggests that certain nutrients exert a direct or indirect effect on amyloid β (Aβ)-peptide production and accumulation [...] Read more.
Alzheimer’s disease (AD) brains are histologically marked by the presence of intracellular and extracellular amyloid deposits, which characterize the onset of the disease pathogenesis. Increasing evidence suggests that certain nutrients exert a direct or indirect effect on amyloid β (Aβ)-peptide production and accumulation and, consequently, on AD pathogenesis. We exploited the fruit fly Drosophila melanogaster model of AD to evaluate in vivo the beneficial properties of Lisosan G, a fermented powder obtained from organic whole grains, on the intracellular Aβ-42 peptide accumulation and related pathological phenotypes of AD. Our data showed that the Lisosan G-enriched diet attenuates the production of neurotoxic Aβ peptides in fly brains and reduces neuronal apoptosis. Notably, Lisosan G exerted anti-oxidant effects, lowering brain levels of reactive oxygen species and enhancing mitochondrial activity. These aspects paralleled the increase in autophagy turnover and the inhibition of nucleolar stress. Our results give support to the use of the Drosophila model not only to investigate the molecular genetic bases of neurodegenerative disease but also to rapidly and reliably test the efficiency of potential therapeutic agents and diet regimens. Full article
(This article belongs to the Special Issue Mitochondrial ROS in Health and Disease)
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14 pages, 2237 KiB  
Article
Exogenous Iron Induces Mitochondrial Lipid Peroxidation, Lipofuscin Accumulation, and Ferroptosis in H9c2 Cardiomyocytes
by Konstantin G. Lyamzaev, He Huan, Alisa A. Panteleeva, Ruben A. Simonyan, Armine V. Avetisyan and Boris V. Chernyak
Biomolecules 2024, 14(6), 730; https://doi.org/10.3390/biom14060730 - 19 Jun 2024
Cited by 2 | Viewed by 1546
Abstract
Lipid peroxidation plays an important role in various pathologies and aging, at least partially mediated by ferroptosis. The role of mitochondrial lipid peroxidation during ferroptosis remains poorly understood. We show that supplementation of exogenous iron in the form of ferric ammonium citrate at [...] Read more.
Lipid peroxidation plays an important role in various pathologies and aging, at least partially mediated by ferroptosis. The role of mitochondrial lipid peroxidation during ferroptosis remains poorly understood. We show that supplementation of exogenous iron in the form of ferric ammonium citrate at submillimolar doses induces production of reactive oxygen species (ROS) and lipid peroxidation in mitochondria that precede ferroptosis in H9c2 cardiomyocytes. The mitochondria-targeted antioxidant SkQ1 and the redox mediator methylene blue, which inhibits the production of ROS in complex I of the mitochondrial electron transport chain, prevent both mitochondrial lipid peroxidation and ferroptosis. SkQ1 and methylene blue also prevented accumulation of lipofuscin observed after 24 h incubation of cardiomyocytes with ferric ammonium citrate. Using isolated cardiac mitochondria as an in vitro ferroptosis model, it was shown that rotenone (complex I inhibitor) in the presence of ferrous iron stimulates lipid peroxidation and lipofuscin accumulation. Our data indicate that ROS generated in complex I stimulate mitochondrial lipid peroxidation, lipofuscin accumulation, and ferroptosis induced by exogenous iron. Full article
(This article belongs to the Special Issue Mitochondrial ROS in Health and Disease)
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Review

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24 pages, 1618 KiB  
Review
Antioxidative Function of Zinc and Its Protection Against the Onset and Progression of Kidney Disease Due to Cadmium
by Soisungwan Satarug
Biomolecules 2025, 15(2), 183; https://doi.org/10.3390/biom15020183 - 27 Jan 2025
Viewed by 458
Abstract
Chronic kidney disease (CKD) is now the world’s top seventh cause of death from a non-communicable disease, and its incidence is projected to increase further as its major risk factors, including obesity, diabetes, hypertension, and non-alcoholic fatty liver disease (NAFLD), continue to rise. [...] Read more.
Chronic kidney disease (CKD) is now the world’s top seventh cause of death from a non-communicable disease, and its incidence is projected to increase further as its major risk factors, including obesity, diabetes, hypertension, and non-alcoholic fatty liver disease (NAFLD), continue to rise. Current evidence has linked the increased prevalence of CKD, diabetes, hypertension, and NAFLD to chronic exposure to the metal pollutant cadmium (Cd). Exposure to Cd is widespread because diet is the main exposure route for most people. Notably, however, the health risk of dietary Cd exposure is underappreciated, and the existing tolerable exposure guidelines for Cd do not afford health protection. New health-protective exposure guidelines are needed. From one’s diet, Cd is absorbed by the intestinal epithelium from where it passes through the liver and accumulates within the kidney tubular epithelial cells. Here, it is bound to metallothionine (MT), and as it is gradually released, it induces tubular damage, tubulointerstitial inflammation and fibrosis, and nephron destruction. The present review provides an update on our knowledge of the exposure levels of Cd that are found to be associated with CKD, NAFLD, and mortality from cardiovascular disease. It discusses the co-existence of hypertension and CKD in people environmentally exposed to Cd. It highlights nuclear and mitochondrial targeting and zinc deficiency as the universal cytotoxic mechanisms of Cd. Special emphasis is placed on the novel antioxidative function of zinc involving de novo heme biosynthesis and the induced expression of heme oxygenase-1 (HO-1). Other exogenous biomolecules with promising anti-Cd toxicity are highlighted. Full article
(This article belongs to the Special Issue Mitochondrial ROS in Health and Disease)
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32 pages, 1987 KiB  
Review
Mitochondrial Reactive Oxygen Species in Infection and Immunity
by Arunima Mukherjee, Krishna Kanta Ghosh, Sabyasachi Chakrabortty, Balázs Gulyás, Parasuraman Padmanabhan and Writoban Basu Ball
Biomolecules 2024, 14(6), 670; https://doi.org/10.3390/biom14060670 - 8 Jun 2024
Cited by 10 | Viewed by 3543
Abstract
Reactive oxygen species (ROS) contain at least one oxygen atom and one or more unpaired electrons and include singlet oxygen, superoxide anion radical, hydroxyl radical, hydroperoxyl radical, and free nitrogen radicals. Intracellular ROS can be formed as a consequence of several factors, including [...] Read more.
Reactive oxygen species (ROS) contain at least one oxygen atom and one or more unpaired electrons and include singlet oxygen, superoxide anion radical, hydroxyl radical, hydroperoxyl radical, and free nitrogen radicals. Intracellular ROS can be formed as a consequence of several factors, including ultra-violet (UV) radiation, electron leakage during aerobic respiration, inflammatory responses mediated by macrophages, and other external stimuli or stress. The enhanced production of ROS is termed oxidative stress and this leads to cellular damage, such as protein carbonylation, lipid peroxidation, deoxyribonucleic acid (DNA) damage, and base modifications. This damage may manifest in various pathological states, including ageing, cancer, neurological diseases, and metabolic disorders like diabetes. On the other hand, the optimum levels of ROS have been implicated in the regulation of many important physiological processes. For example, the ROS generated in the mitochondria (mitochondrial ROS or mt-ROS), as a byproduct of the electron transport chain (ETC), participate in a plethora of physiological functions, which include ageing, cell growth, cell proliferation, and immune response and regulation. In this current review, we will focus on the mechanisms by which mt-ROS regulate different pathways of host immune responses in the context of infection by bacteria, protozoan parasites, viruses, and fungi. We will also discuss how these pathogens, in turn, modulate mt-ROS to evade host immunity. We will conclude by briefly giving an overview of the potential therapeutic approaches involving mt-ROS in infectious diseases. Full article
(This article belongs to the Special Issue Mitochondrial ROS in Health and Disease)
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