Redox Homeostasis and Cellular Adaptation: From Stress Signaling to Defense Strategies

A special issue of Physiologia (ISSN 2673-9488).

Deadline for manuscript submissions: 1 August 2026 | Viewed by 1537

Special Issue Editors


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Guest Editor
Department of Biomedical, Dental and Morphological and Functional Imaging, University of Messina, Messina, Italy
Interests: human physiology; cell physiology; membrane transport systems; bioactive compound; oxidative stress; human health
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98166 Messina, Italy
Interests: human physiology; cell physiology; membrane transport systems; bioactive compounds; oxidative stress; human health
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue welcomes studies addressing various aspects of cellular responses to oxidative stress. We are particularly interested in research on redox homeostasis, mechanisms of ROS generation and detoxification, and the cellular adaptations that preserve physiological functions under oxidative challenges. Contributions exploring intracellular signaling pathways involved in the regulation of cell fate, metabolism, inflammation, and stress tolerance are highly encouraged. 

We also seek submissions focused on antioxidant defense systems, including both endogenous and exogenous compounds, with an emphasis on their mechanisms of action and translational potential. Additionally, we welcome studies investigating the roles of ion channels and membrane transporters in maintaining ionic equilibrium, membrane integrity, metabolic balance, and resilience against oxidative injury.

Finally, particular attention will be given to the structure and function of red blood cells, including erythrocyte membrane organization, hemoglobin-associated redox processes, transport pathways, and intrinsic antioxidant mechanisms that safeguard their physiological performance.

We invite original research articles, reviews, and short communications that provide innovative insights into how cells maintain physiological equilibrium and functional integrity when challenged by oxidative stress.

Dr. Alessia Remigante
Prof. Dr. Rossana Morabito
Dr. Sara Spinelli
Guest Editors

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Keywords

  • oxidative stress
  • antioxidant systems
  • mitochondrial function
  • redox regulation
  • cell signaling

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Published Papers (1 paper)

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Research

22 pages, 4223 KB  
Article
Oxidative Stress-Mediated Effects of Conventional Cigarettes and Heated Tobacco Products on Erythrocyte Membrane Integrity and Regulatory Signaling Pathways
by Sara Spinelli, Elisabetta Straface, Lucrezia Gambardella, Daniele Caruso, Angela Marino, Rossana Morabito and Alessia Remigante
Physiologia 2026, 6(1), 17; https://doi.org/10.3390/physiologia6010017 - 25 Feb 2026
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Abstract
Introduction: cigarette smoking is a major source of systemic oxidative stress and a well-established risk factor for cardiovascular disease. Heated tobacco products (HTPs) are increasingly promoted as reduced-risk alternatives, yet their cellular effects remain incompletely understood. Methods: this study compared the oxidative stress-mediated [...] Read more.
Introduction: cigarette smoking is a major source of systemic oxidative stress and a well-established risk factor for cardiovascular disease. Heated tobacco products (HTPs) are increasingly promoted as reduced-risk alternatives, yet their cellular effects remain incompletely understood. Methods: this study compared the oxidative stress-mediated effects of conventional cigarette smoking and HTP use on human erythrocytes. Erythrocytes from healthy non-smokers, conventional smokers, and HTP users were analyzed using biochemical, functional, and cytological approaches to assess redox status, membrane and cytoskeletal organization, anion exchanger 1 (AE1) function, antioxidant response, and redox-sensitive signaling pathways. Results: conventional smokers exhibited higher intracellular reactive oxygen species (ROS) levels, thiol depletion, methemoglobin and hemichrome formation, whereas HTP users showed marked lipid peroxidation despite lower ROS availability. Both groups instead displayed altered expression and distribution of key membrane and cytoskeletal proteins, including glycophorin A, AE1, spectrin, ankyrin, and band 4.1, indicating impaired membrane–cytoskeleton interactions. Functional analyses revealed an accelerated AE1-mediated anion exchange in erythrocytes from conventional smokers, whereas cells from HTP users exhibited a reduced sulfate accumulation, indicating altered transport capacity. In both groups, G6PDH activity was significantly increased, and redox-sensitive signaling pathways involving ERK, AKT, and eNOS were activated, accompanied by sex-dependent alterations in estrogen receptor expression and distribution. Conclusions: collectively, these findings identify erythrocytes as sensitive biomarkers of tobacco-related systemic damage and indicate that smoking-induced erythrocyte dysfunction, including that associated with HTP use, may actively contribute to vascular impairment. This evidence challenges the assumption that heated tobacco products confer a substantially reduced cardiovascular risk compared with conventional cigarettes. Full article
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