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Antioxidants
Special Issues
Advances in Mitochondrial Redox Biology
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Advances in Mitochondrial Redox Biology

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: 31 August 2024 | Viewed by 9200

Special Issue Editors

Prof. Dr. Gemma Figtree

E-Mail Website
Guest Editor
Northern Clinical School, Kolling Institute of Medical Research, Faculty of Medicine and Health, St Leonards, Australia
Interests: coronary atherosclerosis; inflammation and oxidative stress in the heart and blood vessel; Clinical trials
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Masuko Ushio-Fukai

E-Mail Website
Guest Editor
Vascular Biology Center, Department of Medicine, Cardiology, Medical College of Georgia at Augusta University, Augusta, GA, USA
Interests: reactive oxygen species; redox signaling; vascular endothelial growth factor; angiogenesis; endothelial cells; peripheral arterial disease; diabetes
Special Issues, Collections and Topics in MDPI journals
Dr. Doan Ngo

E-Mail Website1 Website2
Guest Editor
1. School of Biomedical Sciences and Pharmacy, College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, NSW, Australia
2. Hunter Medical Research Institute, New Lambton Heights, Australia
Interests: cardio-oncology; cardiometabolic; obesity; heart failure; redox stress; biomarkers; vascular biology
Special Issues, Collections and Topics in MDPI journals
Dr. Aaron Sverdlov

E-Mail Website1 Website2
Guest Editor
1. School of Medicine and Public Health, College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, NSW, Australia
2. Hunter Medical Research Institute, New Lambton Heights, Australia
Interests: cardio-oncology; cardiometabolic; obesity; heart failure; redox stress; biomarkers; general cardiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondrial function is central to human health. Attaining a deeper understanding of the factors involved in function and dysregulation has long been a focus of researchers committed to the prevention and treatment of disease states including cardiovascular, cardiometabolic, and neurodegenerative diseases, as well as cancer. Current major challenges are related to the obtaining of diagnostic tools to quantify mitochondrial dysfunction, and identify contributing factors, as well as therapeutic tools that can achieve appropriate tissue penetrance and mitochondrial targeting.

We invite researchers to submit original articles or review articles on recent advances in mitochondrial redox biology. Topics include the fundamental biology and physiology of mitochondrial function and signalling, through to novel diagnostics and therapeutics to improve human health.

Prof. Dr. Gemma Figtree
Prof. Dr. Masuko Ushio-Fukai
Dr. Doan Ngo
Dr. Aaron Sverdlov
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
  • mitochondrial biology
  • oxidative stress
  • mitochondrial targeted therapeutics
  • antioxidants
  • cardiometabolic
  • cardiovascular
  • neurodegenerative
  • cancer
  • obesity
  • oxidative signalling

Published Papers (4 papers)

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Research

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18 pages, 13597 KiB  
Article
Melatonin-Mediated Suppression of mtROS-JNK-FOXO1 Pathway Alleviates Hypoxia-Induced Apoptosis in Porcine Granulosa Cells
by Xuan Zhang, Dingding Zhang, Hongmin Li, Zhaojun Liu, Yatong Yang, Jiameng Li, Lishiyuan Tang, Jingli Tao, Honglin Liu and Ming Shen
Antioxidants 2023, 12(10), 1881; https://doi.org/10.3390/antiox12101881 - 19 Oct 2023
Cited by 1 | Viewed by 1063
Abstract
Numerous studies have established that the hypoxic conditions within ovarian follicles induce apoptosis in granulosa cells (GCs), a pivotal hallmark of follicular atresia. Melatonin (N-acetyl-5-methoxytryptamine, MT), a versatile antioxidant naturally present in follicular fluid, acts as a safeguard for maintaining GCs’ survival during [...] Read more.
Numerous studies have established that the hypoxic conditions within ovarian follicles induce apoptosis in granulosa cells (GCs), a pivotal hallmark of follicular atresia. Melatonin (N-acetyl-5-methoxytryptamine, MT), a versatile antioxidant naturally present in follicular fluid, acts as a safeguard for maintaining GCs’ survival during stress exposure. In this study, we unveil an innovative protective mechanism of melatonin against hypoxia-triggered GC apoptosis by selectively inhibiting mitochondrial ROS (mtROS) generation. Specifically, under hypoxic conditions, a gradual accumulation of mitochondrial ROS occurred, consequently activating the JNK-FOXO1 pathway, and driving GCs toward apoptosis. The blocking of JNK or FOXO1 diminished hypoxia-induced GC apoptosis, but this effect was nullified in the presence of GSH, indicating that mtROS instigates apoptosis through the JNK-FOXO1 pathway. Consistent with this, hypoxic GCs treated with melatonin exhibited decreased levels of mtROS, reduced JNK-FOXO1 activation, and mitigated apoptosis. However, the protective capabilities of melatonin were attenuated upon inhibiting its receptor MTNR1B, accompanied by the decreased expression of antioxidant genes. Notably, SOD2, a key mitochondrial antioxidant gene modulated by the melatonin–MTNR1B axis, effectively inhibited the activation of mtROS-JNK-FOXO1 and subsequent apoptosis, whereas SOD2 knockdown abrogated the protective role of melatonin in hypoxic GCs. In conclusion, our study elucidates that melatonin, through MTNR1B activation, fosters SOD2 expression, effectively quelling mtROS-JNK-FOXO1-mediated apoptosis in follicular GCs under hypoxic stress. Full article
(This article belongs to the Special Issue Advances in Mitochondrial Redox Biology)
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17 pages, 7823 KiB  
Article
Overexpression of Mitochondrial Catalase within Adipose Tissue Does Not Confer Systemic Metabolic Protection against Diet-Induced Obesity
by Amanda J. Croft, Conagh Kelly, Dongqing Chen, Tatt Jhong Haw, Aaron L. Sverdlov and Doan T. M. Ngo
Antioxidants 2023, 12(5), 1137; https://doi.org/10.3390/antiox12051137 - 22 May 2023
Cited by 1 | Viewed by 1819
Abstract
Obesity is associated with significant metabolic co-morbidities, such as diabetes, hypertension, and dyslipidaemia, as well as a range of cardiovascular diseases, all of which lead to increased hospitalisations, morbidity, and mortality. Adipose tissue dysfunction caused by chronic nutrient stress can result in oxidative [...] Read more.
Obesity is associated with significant metabolic co-morbidities, such as diabetes, hypertension, and dyslipidaemia, as well as a range of cardiovascular diseases, all of which lead to increased hospitalisations, morbidity, and mortality. Adipose tissue dysfunction caused by chronic nutrient stress can result in oxidative stress, mitochondrial dysfunction, inflammation, hypoxia, and insulin resistance. Thus, we hypothesised that reducing adipose tissue oxidative stress via adipose tissue-targeted overexpression of the antioxidant mitochondrial catalase (mCAT) may improve systemic metabolic function. We crossed mCAT (floxed) and Adipoq-Cre mice to generate mice overexpressing catalase with a mitochondrial targeting sequence predominantly in adipose tissue, designated AdipoQ-mCAT. Under normal diet conditions, the AdipoQ-mCAT transgenic mice demonstrated increased weight gain, adipocyte remodelling, and metabolic dysfunction compared to the wild-type mice. Under obesogenic dietary conditions (16 weeks of high fat/high sucrose feeding), the AdipoQ-mCAT mice did not result in incremental impairment of adipose structure and function but in fact, were protected from further metabolic impairment compared to the obese wild-type mice. While AdipoQ-mCAT overexpression was unable to improve systemic metabolic function per se, our results highlight the critical role of physiological H2O2 signalling in metabolism and adipose tissue function. Full article
(This article belongs to the Special Issue Advances in Mitochondrial Redox Biology)
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15 pages, 2466 KiB  
Article
Impact of Coenzyme Q10 Supplementation on Skeletal Muscle Respiration, Antioxidants, and the Muscle Proteome in Thoroughbred Horses
by Marisa L. Henry, Lauren T. Wesolowski, Joe D. Pagan, Jessica L. Simons, Stephanie J. Valberg and Sarah H. White-Springer
Antioxidants 2023, 12(2), 263; https://doi.org/10.3390/antiox12020263 - 24 Jan 2023
Viewed by 2537
Abstract
Coenzyme Q10 (CoQ10) is an essential component of the mitochondrial electron transfer system and a potent antioxidant. The impact of CoQ10 supplementation on mitochondrial capacities and the muscle proteome is largely unknown. This study determined the effect of CoQ10 supplementation on muscle CoQ10 [...] Read more.
Coenzyme Q10 (CoQ10) is an essential component of the mitochondrial electron transfer system and a potent antioxidant. The impact of CoQ10 supplementation on mitochondrial capacities and the muscle proteome is largely unknown. This study determined the effect of CoQ10 supplementation on muscle CoQ10 concentrations, antioxidant balance, the proteome, and mitochondrial respiratory capacities. In a randomized cross-over design, six Thoroughbred horses received 1600 mg/d CoQ10 or no supplement (control) for 30-d periods separated by a 60-d washout. Muscle samples were taken at the end of each period. Muscle CoQ10 and glutathione (GSH) concentrations were determined using mass spectrometry, antioxidant activities by fluorometry, mitochondrial enzyme activities and oxidative stress by colorimetry, and mitochondrial respiratory capacities by high-resolution respirometry. Data were analyzed using mixed linear models with period, supplementation, and period × supplementation as fixed effects and horse as a repeated effect. Proteomics was performed by tandem mass tag 11-plex analysis and permutation testing with FDR < 0.05. Concentrations of muscle CoQ10 (p = 0.07), GSH (p = 0.75), and malondialdehyde (p = 0.47), as well as activities of superoxide dismutase (p = 0.16) and catalase (p = 0.66), did not differ, whereas glutathione peroxidase activity (p = 0.003) was lower when horses received CoQ10 compared to no supplement. Intrinsic (relative to citrate synthase activity) electron transfer capacity with complex II (ECII) was greater, and the contribution of complex I to maximal electron transfer capacity (FCRPCI and FCRPCIG) was lower when horses received CoQ10 with no impact of CoQ10 on mitochondrial volume density. Decreased expression of subunits in complexes I, III, and IV, as well as tricarboxylic acid cycle (TCA) enzymes, was noted in proteomics when horses received CoQ10. We conclude that with CoQ10 supplementation, decreased expression of TCA cycle enzymes that produce NADH and complex I subunits, which utilize NADH together with enhanced electron transfer capacity via complex II, supports an enhanced reliance on substrates supplying complex II during mitochondrial respiration. Full article
(This article belongs to the Special Issue Advances in Mitochondrial Redox Biology)
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Review

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27 pages, 1734 KiB  
Review
Novel Strategies in the Early Detection and Treatment of Endothelial Cell-Specific Mitochondrial Dysfunction in Coronary Artery Disease
by Weiqian E. Lee, Elijah Genetzakis and Gemma A. Figtree
Antioxidants 2023, 12(7), 1359; https://doi.org/10.3390/antiox12071359 - 28 Jun 2023
Cited by 5 | Viewed by 2712
Abstract
Although elevated cholesterol and other recognised cardiovascular risk factors are important in the development of coronary artery disease (CAD) and heart attack, the susceptibility of humans to this fatal process is distinct from other animals. Mitochondrial dysfunction of cells in the arterial wall, [...] Read more.
Although elevated cholesterol and other recognised cardiovascular risk factors are important in the development of coronary artery disease (CAD) and heart attack, the susceptibility of humans to this fatal process is distinct from other animals. Mitochondrial dysfunction of cells in the arterial wall, particularly the endothelium, has been strongly implicated in the pathogenesis of CAD. In this manuscript, we review the established evidence and mechanisms in detail and explore the potential opportunities arising from analysing mitochondrial function in patient-derived cells such as endothelial colony-forming cells easily cultured from venous blood. We discuss how emerging technology and knowledge may allow us to measure mitochondrial dysfunction as a potential biomarker for diagnosis and risk management. We also discuss the “pros and cons” of animal models of atherosclerosis, and how patient-derived cell models may provide opportunities to develop novel therapies relevant for humans. Finally, we review several targets that potentially alleviate mitochondrial dysfunction working both via direct and indirect mechanisms and evaluate the effect of several classes of compounds in the cardiovascular context. Full article
(This article belongs to the Special Issue Advances in Mitochondrial Redox Biology)
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