Role of Mitochondria and ROS in Health and Disease—2nd Edition

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "ROS, RNS and RSS".

Deadline for manuscript submissions: 28 February 2026 | Viewed by 711

Special Issue Editors


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Guest Editor
Department of Biology, University Federico II of Naples, Via Cinthia 26, 80126 Naples, Italy
Interests: oxidative stress; hyperthyroidism; mitochondria; vitamin E; ROS; antioxidant; insulin resistance

Special Issue Information

Dear Colleagues,

Mitochondria perform a multitude of essential functions within eukaryotic cells and engage in extensive communication with virtually all other cellular organelles. Their primary role is to generate cellular energy through the process of oxidative phosphorylation. This process is intrinsically linked to the production of reactive oxygen species (ROS), molecules that have a hormetic behaviour. While excessive ROS can damage cellular components, including the mitochondria themselves, at controlled levels they serve as important regulators of cellular function.

Mitochondria possess an efficient and adaptable antioxidant defence system able to not only neutralise mitochondrial-derived ROS but also contribute to the detoxification of ROS from other intracellular sources, positioning mitochondria as key regulators of cellular redox homeostasis.

Controlled ROS production plays a critical role in cell signalling, acting as secondary messengers in a range of physiological processes, including adaptation to hypoxia, autophagy regulation, immune response modulation, cellular differentiation, longevity, and metabolic adaptation to physical activity.

Under pathological or stress-related conditions, ROS production can become excessive. This disrupts mitochondrial integrity and initiates a deleterious cycle wherein oxidative damage to components of the respiratory chain, and the Krebs cycle leads to further ROS overproduction. This positive feedback loop amplifies oxidative stress, resulting in widespread cellular injury and functional decline. The progressive accumulation of oxidative damage and loss of mitochondrial integrity are central to the development of numerous non-communicable diseases. These insights underscore the urgent need for a deeper understanding of ROS-related signalling pathways and the identification of strategic molecular targets for effective therapeutic intervention.

We invite you to submit to this second edition of the Special Issue your latest research or a review article aimed at elucidating the fundamental role of mitochondria in modulating cellular ROS dynamics. In addition, the Special Issue’s scope has been broadened to encompass the identification and characterisation of natural bioactive compounds derived from plant and animal-based food matrices that exhibit the capacity of modulating mitochondrial function.

Dr. Paola Venditti
Dr. Gaetana Napolitano
Dr. Gianluca Fasciolo
Guest Editors

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Keywords

  • ROS
  • mitochondria
  • antioxidants
  • oxidative stress
  • neurological diseases
  • metabolic diseases
  • retinal diseases
  • mitochondrial disfunctions
  • mitochondria endoplasmic reticulum communication
  • mitochondrial bioenergetics
  • ageing
  • physical activity

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Published Papers (1 paper)

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Research

22 pages, 3109 KB  
Article
Chlorogenic Acid Alleviates the Detrimental Effects of Concurrent Hyperglycemia and Chronic Stress on Brain Homeostasis by Modulating Antioxidative Defense in Adult Zebrafish
by Rhea Subba, Gianluca Fasciolo, Adriana Petito, Eugenio Geremia, Maria Teresa Muscari Tomajoli, Amal Chandra Mondal, Gaetana Napolitano and Paola Venditti
Antioxidants 2025, 14(12), 1386; https://doi.org/10.3390/antiox14121386 - 21 Nov 2025
Viewed by 503
Abstract
Oxidative stress is a key contributor to diabetes-related cognitive decline and is intensified by diabetes distress (DD), the psychological burden of disease management. DD lowers brain levels of nuclear factor erythroid 2-related factor 2 (NRF2), a transcription factor that regulates antioxidant defense. This [...] Read more.
Oxidative stress is a key contributor to diabetes-related cognitive decline and is intensified by diabetes distress (DD), the psychological burden of disease management. DD lowers brain levels of nuclear factor erythroid 2-related factor 2 (NRF2), a transcription factor that regulates antioxidant defense. This study examined whether chlorogenic acid (CGA), a polyphenolic NRF2 activator, could counteract oxidative and astroglial dysfunctions in adult zebrafish subjected to chronic unpredictable mild stress (CUMS) combined with dextrose, a model mimicking DD. Zebrafish were treated with CGA (50, 100, or 200 mg/kg), and the levels of NRF2 protein and mRNA, along with its regulator keap1, were quantified. Expression levels of key downstream antioxidant genes (sod1, sod2, catalase, glutathione peroxidase, and glutamate-cysteine ligase catalytic subunit) were assessed alongside glutathione (GSH) content and superoxide dismutase (SOD) and catalase activities. Astroglial integrity was evaluated via glial fibrillary acidic protein (GFAP) levels in the whole brain and stress-sensitive regions. CGA increased total brain NRF2 protein, its mRNA, and those of its downstream effectors. At 200 mg/kg, CGA restored GSH levels, boosted antioxidant enzyme activities, and mitigated DD-associated reductions in GFAP and NRF2 in stress-vulnerable areas. These findings identify NRF2 as a promising target to protect brain health under diabetic conditions. Full article
(This article belongs to the Special Issue Role of Mitochondria and ROS in Health and Disease—2nd Edition)
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