Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
5.2
3.9
Journals
Biomedicines
Special Issues
Central Role of Mitochondrial Oxidative Stress in the Pathophysiology of...
share announcement

Central Role of Mitochondrial Oxidative Stress in the Pathophysiology of Disorders

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 December 2024) | Viewed by 10800

Special Issue Editors

Dr. Guilhian Leipnitz

E-Mail Website
Guest Editor
Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre CEP 90035-903, Brazil
Interests: oxidative stress
Special Issues, Collections and Topics in MDPI journals
Dr. André Quincozes-Santos

E-Mail Website
Co-Guest Editor
Departamento de Bioquímica, Universidade Federal do Rio, Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, Bairro Santa Cecília, Porto Alegre 90035-003, RS, Brazil
Interests: oxidative stress; glial cells; neuroprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are the main sites of cellular oxidation and energy conversion, and most cellular ATP is produced by oxidative phosphorylation. During oxidative phosphorylation, reactive oxygen species (ROS) are produced as byproducts in mitochondria, primarily by the respiratory chain complexes I and III, and are sequestered by antioxidant defenses. Mitochondrial functionality is also maintained by the so-called mitochondrial quality control, which includes processes such as mitochondrial biogenesis, dynamics, and mitophagy. Since mitochondria are considered the main source of reactive oxygen species (ROS) production in cells, impairments in bioenergetics or any mitochondrial quality control process are often accompanied by elevated ROS and oxidative damage. Therefore, mitochondrial dysfunction and ROS production are involved in the pathophysiology of primary mitochondrial diseases, neurodegenerative disorders, cardiac insufficiency, diabetes mellitus, and aging, among others. Antioxidants and modulators of mitochondrial function can reduce mitochondrial oxidative damage and are considered promising therapeutic strategies for these pathologies. In this Special Issue, we aim to contribute to a better understanding of the pathophysiology of different pathologies characterized by mitochondrial dysfunction and reveal novel therapeutic approaches for these disorders. We look forward to your contributions to this Special Issue.

Dr. Guilhian Leipnitz
Dr. André Quincozes-Santos
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. Biomedicines 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 2600 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 dysfunction
  • reactive oxygen species
  • bioenergetics
  • mitochondrial quality control
  • pathologies
  • protective agents

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (5 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

15 pages, 2776 KiB  
Article
Obesity-Related Inflammation Reduces Treatment Sensitivity and Promotes Aggressiveness in Luminal Breast Cancer Modulating Oxidative Stress and Mitochondria
by Pere Miquel Morla-Barcelo, Lucas Melguizo-Salom, Pilar Roca, Mercedes Nadal-Serrano, Jorge Sastre-Serra and Margalida Torrens-Mas
Biomedicines 2024, 12(12), 2813; https://doi.org/10.3390/biomedicines12122813 - 11 Dec 2024
Viewed by 1228
Abstract
Background: Obesity, characterized by the secretion of several pro-inflammatory cytokines and hormones, significantly increases the risk of developing breast cancer and is associated with poorer outcomes. Mitochondrial and antioxidant status are crucial in both tumor progression and treatment response. Methods: This study investigates [...] Read more.
Background: Obesity, characterized by the secretion of several pro-inflammatory cytokines and hormones, significantly increases the risk of developing breast cancer and is associated with poorer outcomes. Mitochondrial and antioxidant status are crucial in both tumor progression and treatment response. Methods: This study investigates the impact of an ELIT cocktail (17β-estradiol, leptin, IL-6, and TNFα), which simulates the obesity-related inflammation condition in postmenopausal women, using a 3D culture model. We examined the effects of ELIT exposure on mammosphere formation, oxidative stress and mitochondrial markers, and treatment sensitivity in luminal (T47D, MCF7) and triple-negative (MDA-MB-231) breast cancer cell lines. After that, 3D-derived cells were re-cultured under adherent conditions focusing on the mechanisms leading to dissemination and drug sensitivity. Results: Our results indicated that ELIT condition significantly increased mammosphere formation in luminal breast cancer cell lines (from 3.26% to 6.38% in T47D cell line and 0.68% to 2.32% in MCF7 cell line) but not in the triple-negative MDA-MB-231 cell line. Further analyses revealed a significant decrease in mitochondrial and antioxidant-related markers, particularly in the T47D cell line, where higher levels of ESR2, three-fold increased by ELIT exposure, may play a critical role. Importantly, 3D-derived T47D cells exposed to ELIT showed reduced sensitivity to tamoxifen and paclitaxel, avoiding a 34.2% and 75.1% reduction in viability, respectively. Finally, through in silico studies, we identified specific biomarkers, including TOMM20, NFE2L2, CAT, and ESR2, correlated with poor prognosis in luminal breast cancer. Conclusions: Taken together, our findings suggest that antioxidant and mitochondrial markers are key factors that reduce treatment sensitivity in obesity-related luminal breast cancer. The identified biomarkers may serve as valuable tools for the prognosis and development of more effective therapies in these patients. Full article
(This article belongs to the Special Issue Central Role of Mitochondrial Oxidative Stress in the Pathophysiology of Disorders)
►▼ Show Figures

Figure 1

20 pages, 5699 KiB  
Article
The ABA/LANCL1-2 Hormone/Receptors System Controls ROS Production in Cardiomyocytes through ERRα
by Sonia Spinelli, Lucrezia Guida, Mario Passalacqua, Mirko Magnone, Bujar Caushi, Elena Zocchi and Laura Sturla
Biomedicines 2024, 12(9), 2071; https://doi.org/10.3390/biomedicines12092071 - 11 Sep 2024
Cited by 1 | Viewed by 1123
Abstract
Rat H9c2 cardiomyocytes overexpressing the abscisic acid (ABA) hormone receptors LANCL1 and LANCL2 have an increased mitochondrial proton gradient, respiration, and vitality after hypoxia/reoxygenation. Our aim was to investigate the role of the ABA/LANCL1-2 system in ROS turnover in H9c2 cells. H9c2 cells [...] Read more.
Rat H9c2 cardiomyocytes overexpressing the abscisic acid (ABA) hormone receptors LANCL1 and LANCL2 have an increased mitochondrial proton gradient, respiration, and vitality after hypoxia/reoxygenation. Our aim was to investigate the role of the ABA/LANCL1-2 system in ROS turnover in H9c2 cells. H9c2 cells were retrovirally infected to induce the overexpression or silencing of LANCL1 and LANCL2, without or with the concomitant silencing of the transcription factor ERRα. Enzymes involved in radical production or scavenging were studied by qRT-PCR and Western blot. The mitochondrial proton gradient and ROS were measured with specific fluorescent probes. ROS-generating enzymes decreased, ROS-scavenging enzymes increased, and mitochondrial ROS were reduced in LANCL1/2-overexpressing vs. control cells infected with the empty vector, while the opposite occurred in LANCL1/2-silenced cells. The knockdown of ERRα abrogated all beneficial effects on ROS turnover in LANCL1/2 overexpressing cells. Taken together, these results indicate that the ABA/LANCL1-2 system controls ROS turnover in H9c2 via ERRα. The ABA/LANCL system emerges as a promising target to improve cardiomyocyte mitochondrial function and resilience to oxidative stress. Full article
(This article belongs to the Special Issue Central Role of Mitochondrial Oxidative Stress in the Pathophysiology of Disorders)
►▼ Show Figures

Graphical abstract

13 pages, 3231 KiB  
Article
3-Hydroxy-3-Methylglutaric Acid Disrupts Brain Bioenergetics, Redox Homeostasis, and Mitochondrial Dynamics and Affects Neurodevelopment in Neonatal Wistar Rats
by Josyane de Andrade Silveira, Manuela Bianchin Marcuzzo, Jaqueline Santana da Rosa, Nathalia Simon Kist, Chrístofer Ian Hernandez Hoffmann, Andrey Soares Carvalho, Rafael Teixeira Ribeiro, André Quincozes-Santos, Carlos Alexandre Netto, Moacir Wajner and Guilhian Leipnitz
Biomedicines 2024, 12(7), 1563; https://doi.org/10.3390/biomedicines12071563 - 15 Jul 2024
Cited by 1 | Viewed by 1660
Abstract
3-Hydroxy-3-methylglutaric acidemia (HMGA) is a neurometabolic inherited disorder characterized by the predominant accumulation of 3-hydroxy-3-methylglutaric acid (HMG) in the brain and biological fluids of patients. Symptoms often appear in the first year of life and include mainly neurological manifestations. The neuropathophysiology is not [...] Read more.
3-Hydroxy-3-methylglutaric acidemia (HMGA) is a neurometabolic inherited disorder characterized by the predominant accumulation of 3-hydroxy-3-methylglutaric acid (HMG) in the brain and biological fluids of patients. Symptoms often appear in the first year of life and include mainly neurological manifestations. The neuropathophysiology is not fully elucidated, so we investigated the effects of intracerebroventricular administration of HMG on redox and bioenergetic homeostasis in the cerebral cortex and striatum of neonatal rats. Neurodevelopment parameters were also evaluated. HMG decreased the activity of glutathione reductase (GR) and increased catalase (CAT) in the cerebral cortex. In the striatum, HMG reduced the activities of superoxide dismutase, glutathione peroxidase, CAT, GR, glutathione S-transferase, and glucose-6-phosphate dehydrogenase. Regarding bioenergetics, HMG decreased the activities of succinate dehydrogenase and respiratory chain complexes II–III and IV in the cortex. HMG also decreased the activities of citrate synthase and succinate dehydrogenase, as well as complex IV in the striatum. HMG further increased DRP1 levels in the cortex, indicating mitochondrial fission. Finally, we found that the HMG-injected animals showed impaired performance in all sensorimotor tests examined. Our findings provide evidence that HMG causes oxidative stress, bioenergetic dysfunction, and neurodevelopmental changes in neonatal rats, which may explain the neuropathophysiology of HMGA. Full article
(This article belongs to the Special Issue Central Role of Mitochondrial Oxidative Stress in the Pathophysiology of Disorders)
►▼ Show Figures

Figure 1

Review

Jump to: Research

19 pages, 1199 KiB  
Review
Mitochondrial Dysfunction in Atrial Fibrillation: The Need for a Strong Pharmacological Approach
by Alfredo Mauriello, Adriana Correra, Riccardo Molinari, Gerardo Elia Del Vecchio, Viviana Tessitore, Antonello D’Andrea and Vincenzo Russo
Biomedicines 2024, 12(12), 2720; https://doi.org/10.3390/biomedicines12122720 - 27 Nov 2024
Cited by 3 | Viewed by 1316
Abstract
Despite great progress in treating atrial fibrillation (AF), especially with the development of increasingly effective invasive techniques for AF ablation, many unanswered questions remain regarding the pathogenic mechanism of the arrhythmia and its prevention methods. The development of AF is based on anatomical [...] Read more.
Despite great progress in treating atrial fibrillation (AF), especially with the development of increasingly effective invasive techniques for AF ablation, many unanswered questions remain regarding the pathogenic mechanism of the arrhythmia and its prevention methods. The development of AF is based on anatomical and functional alterations in the cardiomyocyte resulting from altered ionic fluxes and cardiomyocyte electrophysiology. Electric instability and electrical remodeling underlying the arrhythmia may result from oxidative stress, also caused by possible mitochondrial dysfunction. The role of mitochondrial dysfunction in the pathogenesis of AF is not yet fully elucidated; however, the reduction in AF burden after therapeutic interventions that improve mitochondrial fitness tends to support this concept. This selected review aims to summarize the mechanisms of mitochondrial dysfunction related to AF and the current pharmacological treatment options that target mitochondria to prevent or improve the outcome of AF. Full article
(This article belongs to the Special Issue Central Role of Mitochondrial Oxidative Stress in the Pathophysiology of Disorders)
►▼ Show Figures

Graphical abstract

31 pages, 1047 KiB  
Review
Double Trouble: How Microbiome Dysbiosis and Mitochondrial Dysfunction Drive Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis
by Wesam Bahitham, Siraj Alghamdi, Ibrahim Omer, Ali Alsudais, Ilana Hakeem, Arwa Alghamdi, Reema Abualnaja, Faisal M. Sanai, Alexandre S. Rosado and Consolato M. Sergi
Biomedicines 2024, 12(3), 550; https://doi.org/10.3390/biomedicines12030550 - 29 Feb 2024
Cited by 4 | Viewed by 4054
Abstract
Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are closely related liver conditions that have become more prevalent globally. This review examines the intricate interplay between microbiome dysbiosis and mitochondrial dysfunction in the development of NAFLD and NASH. The combination of these [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are closely related liver conditions that have become more prevalent globally. This review examines the intricate interplay between microbiome dysbiosis and mitochondrial dysfunction in the development of NAFLD and NASH. The combination of these two factors creates a synergistic situation referred to as “double trouble”, which promotes the accumulation of lipids in the liver and the subsequent progression from simple steatosis (NAFLD) to inflammation (NASH). Microbiome dysbiosis, characterized by changes in the composition of gut microbes and increased intestinal permeability, contributes to the movement of bacterial products into the liver. It triggers metabolic disturbances and has anti-inflammatory effects. Understanding the complex relationship between microbiome dysbiosis and mitochondrial dysfunction in the development of NAFLD and NASH is crucial for advancing innovative therapeutic approaches that target these underlying mechanisms. Full article
(This article belongs to the Special Issue Central Role of Mitochondrial Oxidative Stress in the Pathophysiology of Disorders)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-5
Back to TopTop