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Cells
Special Issues
Mitochondria Meets Oxidative Stress
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Mitochondria Meets Oxidative Stress

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Mitochondria".

Deadline for manuscript submissions: closed (30 June 2025) | Viewed by 681

Special Issue Editors

Dr. Fernanda M. Ferreira

E-Mail Website
Guest Editor
Department of Agricultural Sciences and Technologies, Agriculture School of Coimbra (ESAC), Polytechnic Institute of Coimbra (IPC), 3045-601 Coimbra, Portugal
Interests: mitochondria; bioenergetics; diabetes; medicinal plants; functional foods
Dr. Francisco Peixoto

E-Mail Website
Guest Editor
Department of Biology and Environment, University of Trás-os-Montes and Alto Douro (UTAD), 5001-801 Vila Real, Portugal
Interests: mitochondria; oxidative stress; reactive oxygen species (ROS); cellular respiration; antioxidant defense
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are crucial in generating cell energy, often celebrated as the cellular powerhouse, despite triggering numerous other critical functions in cell metabolism. However, a delicate equilibrium is disrupted when these tiny organelles face oxidative stress. As both a source and target of reactive oxygen species (ROS), mitochondria become central figures in the intricate dance with oxidative stress. Although ROS are natural byproducts of mitochondrial respiration, elevated levels can damage cellular components. Mitochondria possess sophisticated defense mechanisms to counteract oxidative stress, employing antioxidants and repair systems. The dysfunction of mitochondria due to oxidative stress is associated with various chronical noncommunicable diseases, including neurodegenerative disorders, cardiovascular issues, and ageing. Grasping this intersection is essential for unravelling the complex cellular health and pathology network and aiming to decipher the molecular intricacies that could lead to innovative therapeutic strategies. These strategies may encompass antioxidants, therapies specifically targeting mitochondria, and lifestyle interventions to alleviate oxidative stress and enhance mitochondrial function, thereby mitigating its impact on cellular function and overall health.

Dr. Fernanda M. Ferreira
Dr. Francisco Peixoto
Guest Editors

Manuscript Submission Information

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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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • mitochondria
  • oxidative stress
  • reactive oxygen species (ROS)
  • cellular respiration
  • antioxidant defense
  • ageing

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Published Papers (1 paper)

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Research

23 pages, 9131 KiB  
Article
Mathematical Modeling Unveils a New Role for Transient Mitochondrial Permeability Transition in ROS Damage Prevention
by Olga A. Zagubnaya, Vitaly A. Selivanov, Mark Pekker, Carel J. H. Jonkhout, Yaroslav R. Nartsissov and Marta Cascante
Cells 2025, 14(13), 1006; https://doi.org/10.3390/cells14131006 - 1 Jul 2025
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Abstract
We have previously shown that the mitochondrial respiratory chain (RC) can switch between the following two states: (i) an “ATP-producing” state characterized by the low production of reactive oxygen species (ROS), the vigorous translocation of hydrogen ions (H+), and the storage [...] Read more.
We have previously shown that the mitochondrial respiratory chain (RC) can switch between the following two states: (i) an “ATP-producing” state characterized by the low production of reactive oxygen species (ROS), the vigorous translocation of hydrogen ions (H+), and the storage of energy from the H+ gradient in the form of ATP, and (ii) an “ROS-producing” state, where the translocation of H+ is slow but the production of ROS is high. Here, we suggest that the RC transition from an ATP-producing to an ROS-producing state initiates a mitochondrial permeability transition (MPT) by generating a burst of ROS. Numerous MPT activators induce the transition of the RC to an ROS-producing state, and the ROS generated in this state activate the MPT. The MPT, in turn, induces changes in conditions that are necessary for the RC to return to an ATP-producing state, decreasing the ROS production rate and restoring the normal permeability of the inner membrane. In this way, the transient MPT prevents cell damage from oxidative stress that would occur if the RC remained in an ROS-producing state. It is shown that an overload of glutamate, which enters through excitatory amino acid transporters (EAATs), induces the RC to switch to an ROS-producing state. Subsequent MPT activation causes a transition back to an ATP-producing state. The model was used to predict the spatial–temporal dynamics of glutamate concentrations and H2O2 production rates in a three-dimensional digital phantom of nervous tissue. Full article
(This article belongs to the Special Issue Mitochondria Meets Oxidative Stress)
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