Oxidative Stress in Health and Disease

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 80

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Guest Editor
Department of Medicine and Surgery, University of Enna Kore, Contrada Santa Panasia, 94100 Enna, Italy
Interests: oxidative stress; inflammation; autophagy; metabolic disease; neurodegenerative disease; atherosclerosis; preclinical pharmacology; natural products; flavonoids; cannabinoids; adenosine signaling
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Special Issue Information

Dear Colleagues,

Oxidative stress is caused by an imbalance between the production of oxygen reactive species (ROS), such as superoxide radicals (O2•−), hydrogen peroxide (H2O2), hydroxyl radicals (OH), and singlet oxygen (1O2), and the ability to neutralize them. The accumulation of ROS leads to cellular damage in metabolism processes, negatively affecting several cellular structures and molecules, such as DNA, lipids, and proteins; this can trigger cell inflammation, apoptosis and necrosis, peroxidation, chromosomal aberration, and damage to lipoproteins, membranes, DNA, collagen structure and mitochondrial function. Moreover, oxidative stress is involved in the initiation and progression of numerous diseases, such as cancer, cardiovascular disease, neurological disease, rheumatoid arthritis and autoimmune diseases. Recent studies have demonstrated that elevated ROS levels induce infertility in males and females, impairing the reproductive system. New therapeutic approaches targeting oxidative stress and its signaling molecules could provide the means to treat various human diseases.

This Special Issue of Biomedicines, “Oxidative Stress in Health and Disease”, aims to compile original research papers and cover new literature data and insights on the pathogenesis, molecular pathways and beneficial effects of novel and safe treatments of oxidative stress.

Dr. Federica Mannino
Guest Editor

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Keywords

  • oxidative stress
  • inflammation
  • human diseases
  • apoptosis
  • peroxidation
  • DNA damage
  • mitochondria

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Published Papers (1 paper)

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Review

27 pages, 1619 KiB  
Review
Epigenetic Mechanisms Governing Nrf2 Expression and Its Role in Ferroptosis
by Linbo Li, Xinjun Liu, Zizhen Si and Xidi Wang
Biomedicines 2025, 13(8), 1913; https://doi.org/10.3390/biomedicines13081913 - 5 Aug 2025
Abstract
Ferroptosis is a distinct form of regulated cell death driven by iron-dependent lipid peroxidation participating in various diseases. The nuclear factor erythroid 2-related factor 2 (Nrf2) is a central regulator of cellular redox homeostasis and a key determinant of ferroptosis resistance. Nrf2 activates [...] Read more.
Ferroptosis is a distinct form of regulated cell death driven by iron-dependent lipid peroxidation participating in various diseases. The nuclear factor erythroid 2-related factor 2 (Nrf2) is a central regulator of cellular redox homeostasis and a key determinant of ferroptosis resistance. Nrf2 activates the expression of downstream antioxidant genes to protect cells from oxidative stress and ferroptosis. Consequently, precise regulation of Nrf2 expression is crucial. Recent studies have revealed that complex epigenetic mechanisms involving DNA methylation, histone modifications, and non-coding RNA networks regulate Nrf2 expression. DNA methylation usually suppresses while histone acetylation promotes Nrf2 expression. The influences of histone methylation on NFE2L2 are site- and methylation degree-dependent. m6A modification stabilizes NFE2L2 mRNA to promote Nrf2 expression and thereby inhibit ferroptosis. This article summarizes current understanding of the epigenetic mechanisms controlling Nrf2 expression and Nrf2-mediated ferroptosis pathways and their implications in disease models. The challenges associated with the epigenetic regulation of Nrf2 and future research directions are also discussed. A comprehensive understanding of this regulatory interplay could open new avenues for intervention in ferroptosis-related diseases by fine-tuning cellular redox balance through the epigenetic modulation of Nrf2. Full article
(This article belongs to the Special Issue Oxidative Stress in Health and Disease)
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