Cellular ROS and Antioxidants: Physiological and Pathological Role—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 October 2025 | Viewed by 1019

Special Issue Editors


E-Mail Website
Guest Editor
Ludwig Boltzmann Institute Traumatology, The Research Center in Cooperation with AUVA, 1200 Vienna, Austria
Interests: mitochondrial ROS signaling; oxidative stress; iron metabolism; mitochondrial dysfunction; nitric oxide metabolism; mitochondria targeted antioxidants, TCA cycle; oxoglutarate dehydrogenase complex; shock; inflammation; traumatic brain injury
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Institute of Surgical Research, Albert Szent-Györgyi Medical School, University of Szeged, H-6720 Szeged, Hungary
Interests: hypoxia; ischemia-reperfusion; inflammation; sepsis; biology of gaseous mediators; methane; mitochondria

Special Issue Information

Dear Colleagues,

In the past, reactive oxygen species (ROS) were considered mainly as side products of cellular metabolism that could induce oxidative damage to biomolecules, leading to cellular dysfunction and death. However, studies during the last 30 years have provided strong evidence that ROS play an important role in intracellular signaling and regulate a number of important cellular functions, such as bactericidal activity, metabolic reactions, inflammatory processes, and gene expression. Currently, it is commonly accepted that mitochondrial ROS play a predominant role in orchestrating ROS generated from other sources and regulating the ROS-dependent intracellular metabolism. It should be noted that numerous gas molecules, in addition to oxygen, can participate in these reactions. Moreover, not only are these gasses able to enter the cellular reaction space from the external environment, i.e., from the atmosphere via inhaled air, they can also be produced within the cells or mitochondria during the processes of the "internal combustion" metabolism. These gas-phase intermediates naturally interact with one another through complex and largely unexplored reactions. Consequently, it is appropriate to adopt an approach that considers biologically significant radical reactions as encompassing all biologically relevant gasses. For this Special Issue, we invite submissions that include a balanced consideration of the beneficial and deleterious impacts of ROS, the identification of conditions (ROS types, sources, or threshold concentrations) that differ between the beneficial and deleterious actions of ROS, and considerations of the advantages and disadvantages of antioxidant therapy, with the aim of reducing the severity of disease and facilitating patients’ recovery. A comparison of targeted versus untargeted antioxidants and other mechanistic backgrounds, such as interactions with gas-phase intermediates, will help us to understand the pathophysiological mechanisms underlying ROS-mediated signaling pathways and different cell death mechanisms. For this Special Issue, we invite the submission of original research and review articles.

Prof. Dr. Andrey V. Kozlov
Prof. Dr. Mihály Boros
Dr. Salvatore Nesci
Guest Editors

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. 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

  • reactive oxygen and nitrogen species
  • intracellular signaling
  • oxidative stress
  • iron metabolism
  • mitochondrial dysfunction
  • hypoxia
  • inflammation
  • targeted and untargeted antioxidants
  • gas messengers natural and artificial sources of reactive oxygen species
  • antioxidant defense systems
  • small signaling molecules
  • oxidative stress-driven processes

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

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

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

17 pages, 3505 KiB  
Article
A Novel Hybrid Peptide VLP-Aβ Exhibits Antioxidant Activity In Vitro and In Vivo via KEAP1-NRF2-ARE Signaling Pathway
by Junyong Wang, Wenxiu Zhang, Rijun Zhang, Xuelian Zhao, Jing Zhang, Yichen Zhou, Yucui Tong, Zaheer Abbas, Zhenzhen Li, Haosen Zhang, Di Yang, Sichao Chen, Cong Hu, Dayong Si and Xubiao Wei
Antioxidants 2025, 14(5), 583; https://doi.org/10.3390/antiox14050583 - 12 May 2025
Viewed by 224
Abstract
Oxidative stress plays a crucial role in the development and progression of various diseases. Antioxidant peptides have attracted great attention in agricultural, food, and clinical fields due to their low toxicity, high efficacy, and easy absorption, but the development of antioxidant peptides and [...] Read more.
Oxidative stress plays a crucial role in the development and progression of various diseases. Antioxidant peptides have attracted great attention in agricultural, food, and clinical fields due to their low toxicity, high efficacy, and easy absorption, but the development of antioxidant peptides and their in-depth molecular mechanisms are still lacking. The previous study established a platform for the high-throughput design and screening of multifunctional peptides and successfully identified a novel hybrid peptide, VLP-Aβ (VA), which exhibits both antioxidant and immunomodulatory properties. This study aimed to evaluate the antioxidant activity of VA and investigate the underlying molecular mechanisms. The antioxidant effects of VA were evaluated using both in vitro (H2O2-induced oxidative damage in HepG2 cells) and in vivo (CCl4-induced liver damage in mice) models. VA exhibited significant antioxidant activity both in vitro and in vivo, significantly improving the cell viability and increasing the levels of antioxidant enzymes (SOD, CAT, GSH-Px) to alleviate oxidative stress. These findings indicated that the antioxidant effect of VA is dependent on NRF2, as evidenced by NRF2 knockdown experiments. Further investigation revealed that VA alleviates oxidative stress by modulating the KEAP1-NRF2-ARE signaling pathway. These findings provide insights into the properties of the antioxidant peptide VA, expand the understanding of its molecular mechanisms, and suggest new opportunities for developing VA as a novel functional agent in the agricultural, food, and clinical industries. Full article
Show Figures

Figure 1

17 pages, 3256 KiB  
Article
Replicative Senescence in Mesenchymal Stem Cells: An In Vitro Study on Mitochondrial Dynamics and Metabolic Alterations
by Beatrice Casorati, Isabella Zafferri, Sara Castiglioni and Jeanette A. Maier
Antioxidants 2025, 14(4), 446; https://doi.org/10.3390/antiox14040446 - 8 Apr 2025
Viewed by 538
Abstract
Mesenchymal stem cells (MSCs) are multipotent progenitors capable of self-renewal and differentiation into various cell lineages, making them essential for tissue repair and regenerative medicine. However, their regenerative potential is constrained by replicative senescence, an irreversible growth arrest that occurs after a finite [...] Read more.
Mesenchymal stem cells (MSCs) are multipotent progenitors capable of self-renewal and differentiation into various cell lineages, making them essential for tissue repair and regenerative medicine. However, their regenerative potential is constrained by replicative senescence, an irreversible growth arrest that occurs after a finite number of cell divisions. In this study, we serially passaged human bone marrow-derived MSCs (bMSCs) and compared young, pre-senescent, and senescent cells. The onset of senescence was accompanied by progressive alterations in mitochondrial dynamics, leading to a decline in mitochondrial membrane potential, and increased reactive oxygen species (ROS) production, alongside a diminished cellular antioxidant capacity. These mitochondrial defects play a role in metabolic reprogramming in senescent bMSCs. Our findings underscore the intricate interplay between ROS, mitochondrial dysfunction, and replicative senescence, offering valuable insights to guide the development of therapeutic strategies for preserving MSC functionality in aging and MSC-based therapies. Full article
Show Figures

Figure 1

Back to TopTop