Oxidative Stress and NRF2 in Health and Disease—2nd Edition

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 July 2025 | Viewed by 4307

Special Issue Editor


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Guest Editor
Laboratory for Membrane Transport and Signaling, Division of Molecular Medicine, Ruđer Bošković Institute, HR10000 Zagreb, Croatia
Interests: oxidative stress; reactive oxygen species (ROS); lipid peroxidation; cancer; cancer stem cells; cellular and extracellular antioxidants; NRF2; metabolic reprogramming
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Special Issue Information

Dear Colleagues,

I am delighted to announce that the Special Issue “Oxidative Stress and NRF2 in Health and Disease” is continuing with its 2nd edition, following the success of its 1st edition, which featured numerous excellent papers. These papers are freely accessible at: https://www.mdpi.com/journal/antioxidants/special_issues/H7968G1761.

Oxidative stress (OS) has long been considered a cause of various noncommunicable diseases. The term refers to the increased formation of reactive oxygen species (ROS) and other byproducts that can react with cellular macromolecules such as proteins, DNA, and lipids to impair cellular function. Earlier research opinions assumed that OS only leads to various pathologies and referred to it as a harmful process that should be abolished. However, further research revealed that OS byproducts, such as hydrogen peroxide, are also important for redox signaling. Depending on the cue, cells use their signaling abilities, which include turning certain protein targets on and off, to provide signal transduction that regulates their own functions or the functions of neighboring cells. The extent of OS is closely intertwined with metabolic switches and antioxidant machinery. While some ROS, such as hydrogen peroxide, are essential for normal physiology, their increase leads to pathology. The NRF2 pathway is the main pathway activated as a response to OS. The NRF2 pathway is the major signaling pathway activated in response to OS. The transcription factor NRF2 (nuclear factor, erythroid 2 like 2) is mainly regulated by Kelch-like ECH-associated protein 1 (KEAP1), although its regulation/activation is more complex. NRF2 regulates the expression of more than 250 genes, not only antioxidant enzymes but also others involved in autophagy, metabolism, detoxification, protein turnover, etc. Its mode of action is not always beneficial to humans and is not fully understood.

We invite researchers in this field and participants of the COST Action CA20121 and the Bench to Bedside Transition for Pharmacological regulation of NRF2 in non-communicable diseases (BenBedPhar) to submit their latest research to this Special Issue. Potential topics include, but are not limited to, deciphering the role of oxidative stress and NRF2 in physiology and pathology, their linkage to other signaling pathways, the “omics” approach to identify specific targets and key molecules, potential therapeutic strategies, etc.

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Dr. Lidija Milković
Guest Editor

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Keywords

  • oxidative stress
  • redox signaling
  • NRF2 and its regulation
  • redox-modifying therapeutic approach
  • omics approach
  • physiology
  • non-communicable diseases
  • metabolism
  • aging

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Published Papers (3 papers)

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Research

14 pages, 1023 KiB  
Article
Evidence for a Functional Link Between the Nrf2 Signalling Pathway and Cytoprotective Effect of S-Petasin in Human Retinal Pigment Epithelium Cells Exposed to Oxidative Stress
by Michela Pizzoferrato, Giacomo Lazzarino, Anna Brancato, Elisabetta Tabolacci, Maria Elisabetta Clementi and Giuseppe Tringali
Antioxidants 2025, 14(2), 180; https://doi.org/10.3390/antiox14020180 - 4 Feb 2025
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Abstract
The retinal pigment epithelium (RPE) is a highly specialised monolayer epithelium subjected to constant oxidative stress, which, in the long term, favours the development of a complex pathological process that is the underlying cause of macular damage. Therefore, counteracting the overproduction of ROS [...] Read more.
The retinal pigment epithelium (RPE) is a highly specialised monolayer epithelium subjected to constant oxidative stress, which, in the long term, favours the development of a complex pathological process that is the underlying cause of macular damage. Therefore, counteracting the overproduction of ROS is the best-researched approach to preserve the functional integrity of the RPE. S-Petasin, a secondary metabolite extracted from the plant Petasites hybridus, has numerous biological effects, which highlight its anti-inflammatory and antioxidative properties. The aim of our study is to investigate whether S-Petasin exerts cytoprotective effects by protecting the RPE from oxidative damage. The effects of pretreatment with S-Petasin were assessed by the determination of the cell viability, intracellular ROS levels, activation of the Nrf2 pathway and the resulting post-transcriptional antioxidant/antiapoptotic response. Our results show that S-Petasin pretreatment (1) reduces intracellular ROS levels, improving cell viability of RPE exposed to oxidative damage; (2) activates the Nrf2 signalling pathway, modulating the post-transcriptional response of its antioxidant chemical biomarkers; (3) reduces the Bax levels, and an increase in those of Bcl-2, with a concomitant downregulation of the Bax/Bc-2 ratio. Overall, our results provide the first evidence that S-Petasin is able to protect the RPE from oxidative damage. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease—2nd Edition)
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20 pages, 4339 KiB  
Article
Therapeutic Potential of Dimethyl Fumarate for the Treatment of High-Fat/High-Sucrose Diet-Induced Obesity
by Helber da Maia Valenca, Evelyn Caribé Mota, Andressa Caetano da Fonseca Andrade Silva, Alexsandro Tavares Figueiredo-Junior, Fernanda Verdini, Bruna Romana-Souza, Mariana Renovato-Martins, Manuella Lanzetti, Samuel dos Santos Valenca and João Alfredo Moraes
Antioxidants 2024, 13(12), 1496; https://doi.org/10.3390/antiox13121496 - 8 Dec 2024
Viewed by 1250
Abstract
Obesity is characterized by an imbalance between energy intake and expenditure that triggers abnormal growth of adipose tissues. Dimethyl fumarate (DMF) and its primary active metabolite, monomethyl fumarate (MMF), are Nrf2 activators and have been recognized as strategic antioxidants. This study aimed to [...] Read more.
Obesity is characterized by an imbalance between energy intake and expenditure that triggers abnormal growth of adipose tissues. Dimethyl fumarate (DMF) and its primary active metabolite, monomethyl fumarate (MMF), are Nrf2 activators and have been recognized as strategic antioxidants. This study aimed to evaluate the potential of MMF and DMF to interfere with adipogenesis and obesity, and identify the molecular mechanisms involved. The 3T3-L1 preadipocytes were incubated with differentiation medium (MIX) and simultaneously treated with different concentrations of MMF. In addition, male C57BL/6 mice were fed a standard diet or high-fat/high-sucrose diet (HFHSD) for 16 weeks, during the last 4 of which, they received oral DMF treatment. Exposure to MMF prevented the development of MIX-induced adipogenesis by reducing the expression of transcription factors that drive adipocyte differentiation and by decreasing triglyceride levels. In addition, various antioxidant and anti-inflammatory effects were observed after treatment with MMF as evidenced by the modulation of transcription factor activities and reduction in reactive oxygen species, adipokine, proinflammatory cytokine and resistin levels. In vivo treatment with DMF reduced calorie intake, body weight, and visceral and subcutaneous fat mass in HFHSD mice. Furthermore, DMF administration led to a better glycemic response as well as lower leptin and adiponectin plasma levels in these animals. Our data demonstrate that DMF and its metabolite MMF interfere with adipogenesis and prevent the key features of diet-induced obesity. Considering DMF is already a commercial drug used to treat psoriasis and multiple sclerosis, its pharmacological application for the treatment of obesity and related metabolic disorders holds promise. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease—2nd Edition)
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16 pages, 3292 KiB  
Article
NRF2 and Thioredoxin Reductase 1 as Modulators of Interactions between Zinc and Selenium
by Alina Löser, Maria Schwarz and Anna Patricia Kipp
Antioxidants 2024, 13(10), 1211; https://doi.org/10.3390/antiox13101211 - 8 Oct 2024
Cited by 1 | Viewed by 1634
Abstract
Background: Selenium and zinc are essential trace elements known to regulate cellular processes including redox homeostasis. During inflammation, circulating selenium and zinc concentrations are reduced in parallel, but underlying mechanisms are unknown. Accordingly, we modulated the zinc and selenium supply of HepG2 cells [...] Read more.
Background: Selenium and zinc are essential trace elements known to regulate cellular processes including redox homeostasis. During inflammation, circulating selenium and zinc concentrations are reduced in parallel, but underlying mechanisms are unknown. Accordingly, we modulated the zinc and selenium supply of HepG2 cells to study their relationship. Methods: HepG2 cells were supplied with selenite in combination with a short- or long-term zinc treatment to investigate intracellular concentrations of selenium and zinc together with biomarkers describing their status. In addition, the activation of the redox-sensitive transcription factor NRF2 was analyzed. Results: Zinc not only increased the nuclear translocation of NRF2 after 2 to 6 h but also enhanced the intracellular selenium content after 72 h, when the cells were exposed to both trace elements. In parallel, the activity and expression of the selenoprotein thioredoxin reductase 1 (TXNRD1) increased, while the gene expression of other selenoproteins remained unaffected or was even downregulated. The zinc effects on the selenium concentration and TXNRD activity were reduced in cells with stable NRF2 knockdown in comparison to control cells. Conclusions: This indicates a functional role of NRF2 in mediating the zinc/selenium crosstalk and provides an explanation for the observed unidirectional behavior of selenium and zinc. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Health and Disease—2nd Edition)
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