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

Deadline for manuscript submissions: 31 December 2026 | Viewed by 8475

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Dr. Fotios Tekos

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Department of Biochemistry and Biotechnology, University of Thessaly, Viopolis, Mezourlo, 41500 Larissa, Greece
Interests: redox biology; oxidative stress; antioxidants; cellular signaling; toxicology; inflammation; mitochondrial function; molecular mechanisms of disease; biomedical applications of redox modulation

Special Issue Information

Dear Colleagues,

Redox biology stands at the heart of a wide range of physiological and pathological processes, playing a pivotal role in the maintenance of cellular homeostasis and the progression of numerous diseases. Recent advances have revealed novel insights into redox signaling pathways, antioxidant defense mechanisms, and the therapeutic potential of targeting oxidative stress. This Special Issue, entitled “Current Trends in Redox Physiology Research”, aims to showcase cutting-edge research and comprehensive reviews that enhance our understanding of redox-related mechanisms in health and disease. We welcome contributions addressing molecular and cellular aspects of redox biology, novel biomarkers of oxidative stress, redox-targeted therapies, and the role of nutrition and environmental factors in modulating the redox balance. Experimental and clinical studies are highly encouraged.

We look forward to receiving your valuable contributions that will advance the field of Redox Physiology.

Dr. Fotios Tekos
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 250 words) can be sent to the Editorial Office for assessment.

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Keywords

redox biology
oxidative stress
antioxidant mechanisms
redox signaling
cellular homeostasis
inflammation and redox
nutritional redox modulation
environmental toxicology and redox
mitochondrial dysfunction
oxidative stress biomarkers

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Published Papers (5 papers)

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Research

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17 pages, 2047 KB

Open AccessArticle

Lineage-Dependent Regulation of Glutathione Homeostasis by EAAC1 and GTRAP3-18 During Differentiation of Mesenchymal Stem Cells into Neuron-like Cells

by Nobuko Matsumura, Wattanaporn Bhadhprasit and Koji Aoyama

Int. J. Mol. Sci. 2026, 27(12), 5323; https://doi.org/10.3390/ijms27125323 - 12 Jun 2026

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Abstract

Adult bone marrow-derived mesenchymal stem cells (BMSCs) are multipotent progenitors capable of differentiating into diverse cell lineages, including osteogenic, chondrogenic, adipogenic, and neuronal lineages. In BMSCs, intracellular glutathione (GSH) is a critical determinant of stemness maintenance and differentiation outcomes. However, how intracellular GSH homeostasis is regulated during BMSC-to-neuron differentiation remains unclear. In neurons, GSH synthesis critically depends on cysteine uptake mediated by the excitatory amino acid carrier 1 (EAAC1). Here, we investigated the expression, subcellular localization, and functional contribution of EAAC1 and its regulatory protein, glutamate transporter-associated protein 3-18 (GTRAP3-18) in mouse BMSCs and neuron-like BMSCs generated by Notch intracellular domain-based induction (NICD-3F BMSCs). BMSCs exhibited higher intracellular GSH levels than NICD-3F BMSCs, despite comparable levels of EAAC1 protein. In contrast, EAAC1-dependent cysteine uptake and plasma membrane localization of EAAC1 were markedly reduced in BMSCs, indicating differentiation-dependent regulation of EAAC1 trafficking. Treatment with the xCT inhibitor erastin reduced intracellular GSH levels in both BMSCs and NICD-3F BMSCs. GTRAP3-18 expression was high in BMSCs and significantly reduced in NICD-3F BMSCs. Notably, GTRAP3-18 knockout decreased intracellular GSH levels in BMSCs without altering total EAAC1 protein or intracellular cysteine levels, whereas in NICD-3F BMSCs, both GSH and EAAC1 protein levels were increased. These findings demonstrate lineage-dependent divergence in GSH regulatory mechanisms and reveal previously unrecognized functions of GTRAP3-18 in redox control during stem–to–neuron differentiation. Full article

(This article belongs to the Special Issue Current Trends in Redox Physiology Research)

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19 pages, 1911 KB

Open AccessArticle

Oxy-Inflammatory Profile of Finishers and No-Finishers in an Extreme Ultra-Endurance Trail Race: The 866 km Transpyrénéa

by Simona Mrakic-Sposta, Maristella Gussoni, Federica Mrakic-Sposta, Guido Giardini, Lorenza Pratali, Michela Montorsi, Alessandro Tonacci, Cinzia Dellanoce, Massimo Martinelli and Alessandra Vezzoli

Int. J. Mol. Sci. 2026, 27(10), 4295; https://doi.org/10.3390/ijms27104295 - 12 May 2026

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Abstract

This study investigates the bio-physiological responses occurring under extreme stress conditions and the characterization of the oxy-inflammatory profile of Finishers (FRs) and NoFinishers (NFRs) athletes during the time course and following the Transpyrénéa, an 866 km extreme ultra-race across the French Pyrenees with an altitude difference of 52,900+ m ascent. Thirty-nine experienced ultra-marathon runners (age 43.5 ± 9.1 years; weight 72.1 ± 11.1 kg; BMI 23.3 ± 2.6 kg/m²) were studied using minimally invasive methods on capillary blood and urine samples obtained at baseline (T0), during (T1, 2, 3) and at the end (T4) of the race. Reactive Oxygen Species (ROS) production, total antioxidant capacity (TAC), oxidative damage (8-hydroxy-2-deoxy Guanosine: 8-OH-dG and 8-isoprostane: 8-isoPGF2α), inflammatory (IL-6), nitric oxide pathway (NOx and 3-NT), neopterin, and hematologic (lactate, and hematocrit) biomarkers were assessed. In both FR and NFR athletes a marked systemic increase in ROS, oxidative and nitrosative damage, inflammation, transient immune-renal dysfunction and lactate release were detected throughout the race. Compared to FRs, NFRs displayed significant differences concerning ROS production at T0, 8-isoPGF2-α at T0, T1 and T2, and perceived exertion (RPE score) at T2. These data potentially reflect enhanced adaptative responses to training and metabolic efficacy in FRs, allowing them to better tolerate extreme physiological stress. Full article

(This article belongs to the Special Issue Current Trends in Redox Physiology Research)

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22 pages, 3428 KB

Open AccessArticle

Sex-Specific sRNA Signatures in Rat Liver Reveal Divergent Alterations Following Perinatal Exposure to Glyphosate and Its Mixture with 2,4-D and Dicamba

by Paraskevi Maria Nechalioti, Maria-Anna Kyrgiafini, Periklis Vardakas, Zoi Skaperda, Fotios Tekos, Charitini Nepka, Robin Mesnage, Michael N. Antoniou, Anca Oana Docea, Zissis Mamuris and Demetrios Kouretas

Int. J. Mol. Sci. 2026, 27(10), 4221; https://doi.org/10.3390/ijms27104221 - 9 May 2026

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Abstract

Perinatal exposure to environmental toxicants, even at regulatory relevant doses, can disrupt molecular programming during critical developmental windows, with long-term consequences for organ function and disease risk. We investigated sex-specific hepatic microRNA (miRNA) responses in Wistar rats following perinatal exposure to glyphosate at European Union (EU) acceptable daily intake (ADI) dose (0.5 mg/kg bw/day), at no-observed-adverse-effect level (NOAEL; 50 mg/kg bw/day), and mixed with 2,4-D (0.3 mg/kg bw/day) and dicamba (0.02 mg/kg bw/day), each at their ADI. Using small RNA sequencing, we identified distinct miRNA expression profiles in males and females, with the mixture inducing the most pronounced divergence (52 differentially expressed miRNAs between males and females). Functional enrichment analysis of validated miRNA targets revealed activation of apoptotic, oncogenic, and stress-related pathways in males, alongside downregulation of homeostatic and anti-fibrotic regulators. Females showed suppression of miRNAs involved in hormone signaling, development, and tissue regeneration, suggesting endocrine and adaptive disruption. Our findings highlight the importance of determining effects based on sex and sensitive developmental stages in toxicological assessment, since different regulatory programs may be involved in the response of males and females to xenobiotics. The identified miRNAs may represent early biomarkers of hepatic dysfunction following early-life herbicide exposure, supporting their utility in future risk evaluations. Full article

(This article belongs to the Special Issue Current Trends in Redox Physiology Research)

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Review

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25 pages, 860 KB

Open AccessReview

Targeting Reduced Glutathione (GSH) to Promote Metabolic Health: Insights on the Role of Bioactive-Rich Foods and Fasting Protocols

by Periklis Vardakas, Zoi Skaperda, Paraskevi Maria Nechalioti, Sotiria Makri, Anastasia Patouna, Maria Gkasdrogka, Thomas Karampatzakis, Kyriaki Kroustalli, Georgios Papageorgiou, Evanthia Angeli, Dimitrios Foulos, Fotios Tekos and Demetrios Kouretas

Int. J. Mol. Sci. 2026, 27(14), 6400; https://doi.org/10.3390/ijms27146400 - 18 Jul 2026

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Abstract

The ever-increasing disparity between lifespan and healthspan represents a challenging global issue, with metabolic dysregulation playing a central role in the initiation and progression of chronic non-communicable diseases (NCDs). This review highlights the importance of maintaining optimal redox homeostasis, with particular emphasis on reduced glutathione (GSH), for preserving metabolic health during aging. GSH participates in several physiological processes, including antioxidant defense, xenobiotic detoxification, redox signaling, and metabolic regulation. Diminished GSH levels are consistently reported in obesity, insulin resistance, type 2 diabetes mellitus, non-alcoholic fatty liver, and cardiovascular diseases. Current evidence from human clinical studies indicates that foods rich in bioactive constituents can enhance GSH levels and stimulate GSH-dependent enzyme activity, with the Nrf2/Are signaling pathway being a central mechanistic link. Fasting may promote adaptive redox responses by inducing mild oxidative stress and activating the same molecular mechanism, although the effects on GSH-related antioxidant mechanisms remain heterogeneous across fasting protocols and study populations. Altogether, the available clinical evidence suggests that these nutritional and lifestyle interventions exhibit more consistent beneficial effects in individuals characterized by increased oxidative burden and underlying metabolic dysfunction. Interindividual differences in GSH responses further underscore the need for targeted, tailor-made approaches that account for genetic, epigenetic, and lifestyle factors. Collectively, targeting GSH homeostasis through nutritional and lifestyle interventions represents a promising strategy for improving metabolic health and may further contribute to healthy aging, positioning redox biology at the forefront of aging research and NCD prevention. Full article

(This article belongs to the Special Issue Current Trends in Redox Physiology Research)

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47 pages, 2124 KB

Open AccessReview

From Electron Imbalance to Network Collapse: Decoding the Redox Code of Ischemic Stroke for Biomarker-Guided Precision Neuroprotection

by Ionut Bogdan Diaconescu, Adrian Vasile Dumitru, Calin Petru Tataru, Corneliu Toader, Matei Șerban, Răzvan-Adrian Covache-Busuioc and Lucian Eva

Int. J. Mol. Sci. 2025, 26(22), 10835; https://doi.org/10.3390/ijms262210835 - 7 Nov 2025

Cited by 18 | Viewed by 3891

Abstract

Ischemic stroke remains one of the most catastrophic diseases in neurology, in which, due to a disturbance in the cerebral blood flow, the brain is acutely deprived of its oxygen and glucose oligomer, which in turn rapidly leads to energetic collapse and progressive cellular death. There is now increasing evidence that this type of stroke is not simply a type of ‘oxidative stress’ but rather a programmable loss-of-redox homeostasis, within which electron flow and the balance of oxidants/reductants are cumulatively displaced at the level of the single molecule and at the level of the cellular area. The advances being made in cryo-electron microscopy, lipidomics, and spatial omics are coupled with the introduction of a redox code produced by the interaction of the couples NADH/NAD⁺, NADPH/NADP⁺, GSH/GSSG, BH₄/BH₂, and NO/SNO, which determine the end results of the fates of the neurons, glia, endothelium, and pericytes. Within the mitochondria, pathophysiological events, including reverse electron transport, succinate overflow, and permeability transition, are found to be the first events after reperfusion, while signals intercommunicating via ER–mitochondria contact, peroxisomes, and nanotunnels control injury propagation. At the level of the tissue, events such as the constriction of the pericytes, the degradation of the glycocalyx, and the formation of neutrophil extracellular traps underlie microvascular failure (at least), despite the effective recanalization of the vessels. Systemic influences such as microbiome products, oxidized lipids, and free mitochondrial DNA in cells determine the redox imbalance, but this generally occurs outside the brain. We aim to synthesize how the progressive stages of ischemic injury evolve from the cessation of flow to the collapse of the cell structure. Within seconds of injury, there is reverse electron transport (RET) through mitochondrial complex I, with bursts of superoxide (O₂•⁻) and hydrogen peroxide (H₂O₂) being produced, which depletes the stores of superoxide dismutase, catalase, and glutathione peroxidase. Accumulated succinate and iron-induced lipid peroxidation trigger ferroptosis, while xanthine oxidase and NOX2/NOX4, as well as uncoupled eNOS/nNOS, lead to oxidative and nitrosative stress. These cascades compromise the function of neuronal mitochondria, the glial antioxidant capacity, and endothelial–pericyte integrity, leading to the degradation of the glycocalyx with microvascular constriction. Stroke, therefore, represents a continuum of redox disequilibrium, a coordinated biochemical failure linking the mitochondrial metabolism with membrane integrity and vascular homeostasis. Full article

(This article belongs to the Special Issue Current Trends in Redox Physiology Research)

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