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Oxidative Stress: Cell Biology and Signal Transduction

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 April 2025) | Viewed by 6229

Special Issue Editors


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Guest Editor
Department of Anatomy, Cell Biology and Zoology, Science Faculty, University of Extremadura, 06006 Badajoz, Spain
Interests: oxidative stress; apoptosis; biophysics; calcium signalling; cell biology; developmental biology

E-Mail Website
Guest Editor
Grupo de Investigación Neuroinmunofisiología y Crononutrición, Departamento de Fisiología, Facultad de Ciencias, Universidad de Extremadura, Avenida de Elvas s/n, 06006 Badajoz, Spain
Interests: cancer biology; antioxidants; reactive oxygen species; molecular biology; mitochondria; cancer therapy
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Special Issue Information

Dear Colleagues,

Oxidative stress is a process of high interest for researchers around the world. Diverse signal recognition receptors and signal transduction pathways have been defined that regulate mitochondrial functions, apoptosis, and development. A perturbation of the equilibrium between reactive oxygen species (ROS) and antioxidant molecules in the cell leads to signalling pathways that cause pathophysiological processes and diseases. Therefore, the understanding of the diverse signalling molecules, signal recognition mechanisms, and signal transduction pathways is fundamental for gaining insight into physiological and pathophysiological processes. This open access Special Issue will combine original research and review articles on oxidative stress. It highlights discoveries, approaches, and technical developments in oxidative stress research with a special interest in molecular data. The main feature of this Special Issue is to advance our understanding of oxidative stress processes in several diseases, which may lead to the discovery of novel molecular diagnostic technologies and targeted therapeutics.

Therefore, authors are invited to submit original research and review articles that address the progress and current standing of cellular signalling processes.

Topics of this Special Issue include, but are not limited to:

  • Key biological processes such as cell cycle, DNA repair, apoptosis, autophagy, angiogenesis, invasion and metastasis.
  • Mitochondrial mechanisms.
  • Degenerative diseases.
  • Cancer epidemiology and prevention.
  • Oxidative agents and their molecular effects.
  • Antioxidant therapy: target discovery, drug design, nutrition, targeted therapy, nanomaterials, personalized medicine.

Dr. David González-Flores
Dr. Javier Espino
Guest Editors

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • signalling molecules
  • reactive oxygen species
  • apoptosis
  • signal transduction
  • signalling network
  • second messenger
  • antioxidant molecules
  • oxidant agents

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Published Papers (4 papers)

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Research

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18 pages, 2722 KiB  
Article
5G Radiofrequency Exposure Reduces PRDM16 and C/EBP β mRNA Expression, Two Key Biomarkers for Brown Adipogenesis
by Chandreshwar Seewooruttun, Bélir Bouguila, Aurélie Corona, Stéphane Delanaud, Raphaël Bodin, Véronique Bach, Rachel Desailloud and Amandine Pelletier
Int. J. Mol. Sci. 2025, 26(6), 2792; https://doi.org/10.3390/ijms26062792 - 20 Mar 2025
Viewed by 678
Abstract
The widespread use of wireless technologies has raised public health concerns about the biological effects of radiofrequency (RF) exposure. Children have a higher specific absorption rate (SAR) of radiation energy compared to adults. Furthermore, brown adipose tissue (BAT) is more prevalent in infants [...] Read more.
The widespread use of wireless technologies has raised public health concerns about the biological effects of radiofrequency (RF) exposure. Children have a higher specific absorption rate (SAR) of radiation energy compared to adults. Furthermore, brown adipose tissue (BAT) is more prevalent in infants and tends to decrease with age. Previous animal studies demonstrated a cold sensation in rats exposed to 900 MHz (second generation, 2G). UCP1-dependent thermogenesis and BAT hyperplasia are two fundamental adaptive mechanisms initiated in response to cold. This study investigated the impact of short-term exposure to 2G and fifth generation (5G) on key thermogenic and adipogenic markers related to these mechanisms while considering age and exposure duration. Juvenile and young adult Wistar rats were randomized into three subgroups: a 5G group (3.5 GHz), 2G group (900 MHz), and a control group (SHAM). They were exposed to their respective continuous-wave RF signals for 1 or 2 weeks at an intensity of 1.5 V/m, with two exposure sessions of 1 h per day. After the exposure period, a RT-qPCR was carried out to evaluate the genetic markers involved in BAT thermogenesis and adipogenesis. Two adipogenic biomarkers were affected; a fold change reduction of 49% and 32% was detected for PRDM16 (p = 0.016) and C/EBP β (p = 0.0002), respectively, after 5G exposure, regardless of age and exposure duration. No significant RF effect was found on UCP1-dependent thermogenesis at a transcriptional level. These findings suggest that exposure to a 5G radiofrequency may partially disrupt brown adipocyte differentiation and thermogenic function by downregulating PRDM16 and C/EBP β, possibly leading to higher cold sensitivity. Full article
(This article belongs to the Special Issue Oxidative Stress: Cell Biology and Signal Transduction)
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16 pages, 2747 KiB  
Article
The Transcription Factor StuA Regulates Oxidative Stress-Responsive Genes in Trichophyton rubrum
by Monise Fazolin Petrucelli, Leonardo Martins-Santana, Vanderci M. Oliveira, Pablo R. Sanches, Antonio Rossi and Nilce M. Martinez-Rossi
Int. J. Mol. Sci. 2024, 25(23), 12959; https://doi.org/10.3390/ijms252312959 - 2 Dec 2024
Viewed by 830
Abstract
Fungi can remarkably sense and adapt to various extracellular stimuli and stress conditions. Oxidative stress, which results from an imbalance between reactive oxygen species production and antioxidant defenses, leads to cellular damage and death. In Trichophyton rubrum, oxidative stress is managed by [...] Read more.
Fungi can remarkably sense and adapt to various extracellular stimuli and stress conditions. Oxidative stress, which results from an imbalance between reactive oxygen species production and antioxidant defenses, leads to cellular damage and death. In Trichophyton rubrum, oxidative stress is managed by a complex antioxidant system, including thioredoxins, glutathione, catalases, peroxidases, and superoxide dismutase, with glutathione playing a crucial role. The fungus also responds to oxidative stress through critical pathways such as the glycerol high-osmolarity pathway, activator protein 1 transcription factor, and responsive regulator SKN7. To better understand the role of the transcription factor StuA in regulating oxidative stress-related genes within these pathways, we conducted gene expression studies in ΔstuA mutant and wild-type strains of T. rubrum cultivated in keratin and under oxidative stress induced by hydrogen peroxide. Our results revealed significant downregulation of essential antioxidant genes, including glutathione transferases and catalases, in the ΔstuA mutant. Moreover, catalase and glutathione S-transferase activities were impaired in the mutants under stress conditions, highlighting the impact of this mutation. These findings underscore the critical role of StuA in the oxidative stress response and fungal pathogenesis and provide new insights into T. rubrum’s adaptive mechanisms. Full article
(This article belongs to the Special Issue Oxidative Stress: Cell Biology and Signal Transduction)
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Review

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28 pages, 4435 KiB  
Review
Reactive Oxygen Species (ROS) in Metabolic Disease—Don’t Shoot the Metabolic Messenger
by Ross T. Lindsay and Christopher J. Rhodes
Int. J. Mol. Sci. 2025, 26(6), 2622; https://doi.org/10.3390/ijms26062622 - 14 Mar 2025
Cited by 1 | Viewed by 713
Abstract
Reactive oxygen species (ROS) are widely considered key to pathogenesis in chronic metabolic disease. Consequently, much attention is rightly focused on minimising oxidative damage. However, for ROS production to be most effectively modulated, it is crucial to first appreciate that ROS do not [...] Read more.
Reactive oxygen species (ROS) are widely considered key to pathogenesis in chronic metabolic disease. Consequently, much attention is rightly focused on minimising oxidative damage. However, for ROS production to be most effectively modulated, it is crucial to first appreciate that ROS do not solely function as pathological mediators. There are >90 gene products specifically evolved to generate, handle, and tightly buffer the cellular concentration of ROS. Therefore, it is likely that ROS plays a role as integral homeostatic signalling components and only become toxic in extremis. This review explores these commonly overlooked normal physiological functions, including how ROS are generated in response to environmental or hormonal stimuli, the mechanisms by which the signals are propagated and regulated, and how the cell effectively brings the signal to an end after an appropriate duration. In the course of this, several specific and better-characterised signalling mechanisms that rely upon ROS are explored, and the threshold at which ROS cross from beneficial signalling molecules to pathology mediators is discussed. Full article
(This article belongs to the Special Issue Oxidative Stress: Cell Biology and Signal Transduction)
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21 pages, 838 KiB  
Review
Oxidative Effects in Early Stages of Embryo Development Due to Alcohol Consumption
by David González-Flores, Antonia Márquez and Ilda Casimiro
Int. J. Mol. Sci. 2024, 25(7), 4100; https://doi.org/10.3390/ijms25074100 - 7 Apr 2024
Cited by 4 | Viewed by 3237
Abstract
Alcohol, a widely consumed drug, exerts significant toxic effects on the human organism. This review focuses on its impact during fetal development, when it leads to a spectrum of disorders collectively termed Fetal Alcohol Spectrum Disorders (FASD). Children afflicted by FASD exhibit distinct [...] Read more.
Alcohol, a widely consumed drug, exerts significant toxic effects on the human organism. This review focuses on its impact during fetal development, when it leads to a spectrum of disorders collectively termed Fetal Alcohol Spectrum Disorders (FASD). Children afflicted by FASD exhibit distinct clinical manifestations, including facial dysmorphism, delayed growth, and neurological and behavioral disorders. These behavioral issues encompass diminished intellectual capacity, memory impairment, and heightened impulsiveness. While the precise mechanisms underlying alcohol-induced fetal damage remain incompletely understood, research indicates a pivotal role for reactive oxygen species (ROS) that are released during alcohol metabolism, inciting inflammation at the cerebral level. Ethanol metabolism amplifies the generation of oxidant molecules, inducing through alterations in enzymatic and non-enzymatic systems responsible for cellular homeostasis. Alcohol consumption disrupts endogenous enzyme activity and fosters lipid peroxidation in consumers, potentially affecting the developing fetus. Addressing this concern, administration of metformin during the prenatal period, corresponding to the third trimester of human pregnancy, emerges as a potential therapeutic intervention for mitigating FASD. This proposed approach holds promise for ameliorating the adverse effects of alcohol exposure on fetal development and warrants further investigation. Full article
(This article belongs to the Special Issue Oxidative Stress: Cell Biology and Signal Transduction)
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