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Antioxidants
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Modulation of Biochemical, Cellular and Physiological Mechanisms in Response to...
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Modulation of Biochemical, Cellular and Physiological Mechanisms in Response to Oxidative Stress in Animals

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: 15 September 2026 | Viewed by 5108

Special Issue Editors

Dr. Konstantinos Feidantsis

E-Mail Website
Guest Editor
Department of Fisheries & Aquaculture, University of Patras, Mesolonghi, Greece
Interests: animal physiology; cell physiology; comparative physiology; environmental physiology; cell signaling; climate change; bioindicators
Special Issues, Collections and Topics in MDPI journals
Dr. Vasiliki Sapanidou

E-Mail Website
Guest Editor Assistant
Laboratory of Animal Physiology, School of Veterinary Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece
Interests: assisted reproductive techniques; cryopreservation; embryos; flow cytometry; sperm; oocytes; fertility; oocyte vitrification; reactive oxygen species; melatonin

Special Issue Information

Dear Colleagues,

Oxidative stress has profound effects on biochemical, cellular, and physiological processes. If oxidative stress is not ameliorated, it may result in irreversible oxidative damage to macromolecules and cellular components, thus contributing to the pathogenesis of various conditions and diseases, as well as aging. Oxidative stress is implicated in animals’ health and welfare through multiple ways, such as cellular signaling, cell death pathways as apoptosis and ferroptosis, autophagy, inflammation, and metabolic dysregulation. The regulation of these cellular pathways by several internal and external factors, such as enzymatic or non-enzymatic antioxidants, may ensure the timely response of cells and subsequently their prolonged stamina against oxidative stress. The elucidation of these underlying mechanisms is crucial for developing strategies to mitigate oxidative stress and its associated welfare and health risks in animals.

For this reason, we kindly invite you to submit your original research papers and reviews to the Special Issue “Modulation of Biochemical, Cellular and Physiological Mechanisms in Response to Oxidative Stress in Animals”, with the aim to better comprehend the complex relationship between oxidative stress and the regulatory mechanisms that participate in cellular function and disease processes.

Dr. Konstantinos Feidantsis
Guest Editor

Dr. Vasiliki Sapanidou
Guest Editor Assistant

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.

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. Antioxidants 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 2900 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

  • animals
  • cell signaling
  • metabolism
  • cell death responses
  • oxidative damage

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

Published Papers (3 papers)

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Research

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21 pages, 3050 KB  
Article
2-Methoxystypandrone from Polygonum cuspidatum Rejuvenates Senescence by Reducing Mitochondrial ROS
by Jee Hee Yoon, Ye Hyang Kim, Minseon Kim, Eun Young Jeong, Yun Haeng Lee, Ji Ho Park, Yoo Jin Lee, So Hun Lee, Ha Yeon Kim, Hye Min Kang, Hyung Wook Kwon, Youngjoo Byun, Song Seok Shin and Joon Tae Park
Antioxidants 2026, 15(3), 357; https://doi.org/10.3390/antiox15030357 - 11 Mar 2026
Viewed by 856
Abstract
Oxidative stress induced by reactive oxygen species (ROS) is a major contributor to senescence. Although strategies to mitigate ROS are considered crucial for reversing this process, effective interventions remain limited. Extracts from Polygonum cuspidatum (P. cuspidatum) have shown protective effects against [...] Read more.
Oxidative stress induced by reactive oxygen species (ROS) is a major contributor to senescence. Although strategies to mitigate ROS are considered crucial for reversing this process, effective interventions remain limited. Extracts from Polygonum cuspidatum (P. cuspidatum) have shown protective effects against senescence by suppressing mitochondrial ROS production; however, the specific bioactive compound responsible for these effects has not yet been identified. This study aimed to identify the active compound in P. cuspidatum responsible for reducing mitochondrial ROS and to elucidate its mechanism of action in rejuvenating senescence. Bioactive components of P. cuspidatum extract were screened for their ability to decrease mitochondrial ROS production. The most potent compound, 2-methoxystypandrone (2-MS), was further examined for its effects on oxidative phosphorylation (OXPHOS) efficiency, mitochondrial ROS generation, and senescence-associated phenotypes in a skin cell-based model. 2-MS was identified as the most effective compound for reducing mitochondrial ROS. Mechanistically, 2-MS enhanced OXPHOS efficiency, thereby minimizing ROS production resulting from inefficient respiration. Reduction in mitochondrial ROS by 2-MS restored senescence-associated phenotypes and rejuvenated senescence by suppressing ROS-driven melanogenesis and inflammatory responses in skin cells. This study identifies 2-MS as a key active ingredient of P. cuspidatum that exerts anti-aging effects through the reduction in mitochondrial ROS generation. These findings highlight 2-MS as a promising therapeutic and cosmetic candidate for rejuvenating senescence. Full article
(This article belongs to the Special Issue Modulation of Biochemical, Cellular and Physiological Mechanisms in Response to Oxidative Stress in Animals)
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17 pages, 2070 KB  
Article
Molecular Insights into the Genesis of Heat Hardening in Marine Bivalves
by Ioannis Georgoulis, Ioannis A. Giantsis, Basile Michaelidis, Athanasios Kouniakis and Konstantinos Feidantsis
Antioxidants 2025, 14(12), 1468; https://doi.org/10.3390/antiox14121468 - 7 Dec 2025
Cited by 2 | Viewed by 843
Abstract
Heat hardening induces complex biochemical reprogramming that enhances thermal resilience in marine bivalves. Despite this technique’s promising results in marine animals, the molecular basis of heat hardening is far from understood. This study elucidates the molecular mechanisms underlying the hardening process in Mytilus [...] Read more.
Heat hardening induces complex biochemical reprogramming that enhances thermal resilience in marine bivalves. Despite this technique’s promising results in marine animals, the molecular basis of heat hardening is far from understood. This study elucidates the molecular mechanisms underlying the hardening process in Mytilus galloprovincialis exposed to a 4-day sublethal heat treatment. Induction of hsf-1, hsp70, and hsp90 genes revealed the activation of the heat shock response and proteostasis machinery, ensuring proper protein folding and preventing oxidative and proteotoxic stress. Simultaneous upregulation of mitochondrial (atpase6, cox1, nadh) and glycolytic (pk, cs) genes reflects enhanced oxidative phosphorylation and glycolytic flux, maintaining ATP supply and metabolic flexibility under elevated temperatures. Increased hif-1α expression suggests transient hypoxia signaling, coordinating oxygen utilization with redox control. Reinforcement of antioxidant defenses, together with elevated autophagy-related transcription, denotes a shift toward oxidative stress mitigation and damaged organelle clearance. Balanced expression of pro- (bax) and anti-apoptotic (bcl-2) factors, along with nf-κb modulation, supports tight regulation of cell survival and inflammatory responses. These findings underscore a highly integrated biochemical network linking proteostasis, intermediary metabolism, redox balance, and antioxidant defense with cellular quality control, which together underpin the physiological plasticity of heat-hardened M. galloprovincialis, enhancing survival under transient thermal stress. Full article
(This article belongs to the Special Issue Modulation of Biochemical, Cellular and Physiological Mechanisms in Response to Oxidative Stress in Animals)
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Review

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29 pages, 3761 KB  
Review
SHP2: A Redox-Sensitive Regulator Linking Immune Checkpoint Inhibitor Therapy to Cancer Treatment and Vascular Risk
by Silvia Fernanda López Moreno, Stefania Assunto Lenz, Bernardo Casso-Chapa, Angelica Paniagua-Bojorges, Jung Hyun Kim, Nicolas L. Palaskas, Kevin T. Nead, Venkata S. K. Samanthapudi, Gilbert Mejia, Oanh Hoang, Jonghae Lee, Steven H. Lin, Joerg Herrmann, Guangyu Wang, Syed Wamique Yusuf, Cezar A. Iliescu, Noah I. Beinart, Charlotte Manisty, Masuko Ushio-Fukai, Tohru Fukai, Pietro Ameri, Roza I. Nurieva, Michelle A. T. Hildebrandt, Keri Schadler, Efstratios Koutroumpakis, Sivareddy Kotla, Nhat-Tu Le and Jun-ichi Abeadd Show full author list remove Hide full author list
Antioxidants 2025, 14(12), 1388; https://doi.org/10.3390/antiox14121388 - 21 Nov 2025
Cited by 1 | Viewed by 2608
Abstract
Src homology 2-domain containing protein tyrosine phosphatase 2 (SHP2), encoded by the Ptpn11 gene (Tyrosine-protein phosphatase non-receptor type 11), is a key downstream effector of PD-1/PD-L1 signaling and is likely important, in addition to immune modulation, in tumor development and vascular homeostasis. SHP2 [...] Read more.
Src homology 2-domain containing protein tyrosine phosphatase 2 (SHP2), encoded by the Ptpn11 gene (Tyrosine-protein phosphatase non-receptor type 11), is a key downstream effector of PD-1/PD-L1 signaling and is likely important, in addition to immune modulation, in tumor development and vascular homeostasis. SHP2 conveys PD-1 mediated inhibitory signaling in T cells, and is emerging as a therapeutic target. Importantly, there is an association between immune checkpoint inhibitors (ICIs), immune-related adverse events (irAEs), and cardiovascular complications, underscoring the need to understand SHP2’s role in these processes. This review aims to summarize current knowledge on SHP2/PTPN11 biology, its role in immune regulation, cancer progression, and vascular homeostasis, and to discuss emerging therapeutic strategies targeting this pathway. The concept of using SHP2 inhibitors with immune checkpoint inhibitors (ICIs) is being investigated to address ICI resistance and to improve anti-tumor efficacy substantially. SHP2 is also being studied in non-cancer cell contexts, and signaling responses can differ by large magnitudes depending on the biological context and stimuli. Under normal circumstances, SHP2 promotes vascular homeostasis in endothelial cells (ECs) and myeloid cells and inhibits inflammation, and the reduction in SHP2 activity by oxidative stress, such as in atherosclerosis or diabetes, upregulates inflammation. In contrast, in response to radiation, the fibrotic response and subsequent lung injury were increased by endothelial SHP2 induction via Notch-Jag1 signaling. Vascular smooth muscle cells SHP2 act as a pro-atherogenic effector by enhancing ERK/MAPK signaling, and the upregulation of mitochondria localized SHP2 can also induce cellular senescence-associated inflammation by upregulating mitochondrial reactive oxygen species. Taken together, the two opposite signaling effects of SHP2 suggest that both the immune and vascular system responses appear to be more modulated by the redox, cell, and compartment-specific signaling of SHP2. More studies are needed for mitigating cardiovascular toxicity to patients, particularly with ICI-based treatment regimens. Full article
(This article belongs to the Special Issue Modulation of Biochemical, Cellular and Physiological Mechanisms in Response to Oxidative Stress in Animals)
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