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Current Trends in Redox Physiology Research
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Current Trends in Redox Physiology Research

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

Deadline for manuscript submissions: 20 April 2026 | Viewed by 1613

Special Issue Editor

Dr. Fotios Tekos

E-Mail Website
Guest Editor
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 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • 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 (1 paper)

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Review

47 pages, 2124 KB  
Review
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 (registering DOI) - 7 Nov 2025
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 [...] Read more.
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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