Redox Resilience in Mitochondrial Health and Disease: New Advances in Cellular Defense Mechanisms

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: 15 March 2026 | Viewed by 399

Special Issue Editors


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Laboratory of Mucosal Exposome and Biomodulation, Department of Integrative Biomedical Sciences, Biomedical Research Institute, Pusan National University, Yangsan 50612, Republic of Korea
Interests: systems toxicology; metabolic stress; ribosome; mucosal immunology
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Guest Editor
1. Department of Obstetrics and Gynecology, School of Medicine, Pusan National University, Busan 46241, Republic of Korea
2. Biomedical Research Institute, Pusan National University Hospital, Busan 49241, Republic of Korea
Interests: cancer; endometriosis; molecular mechanism; metabolic stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria, as the powerhouses of the cell, play a central role in both energy production and cellular homeostasis. Emerging research highlights the crucial role of mitochondrial redox resilience in preserving mitochondrial health, particularly in response to oxidative stress and metabolic challenges. The concept of redox resilience—defined as the capacity of mitochondria to sustain redox homeostasis despite fluctuating environmental and cellular conditions—has profound implications for understanding cellular aging, neurodegenerative diseases, metabolic disorders, and cancer. 

This topic aims to explore the molecular mechanisms underlying mitochondrial redox resilience, focusing on how mitochondria manage oxidative damage, facilitate metabolic reprogramming, and coordinate protective pathways. Investigating mitochondrial redox-sensitive pathways and the interplay between mitochondrial dynamics and cellular stress responses will open new avenues for therapeutic interventions. Additionally, understanding how mitochondrial redox resilience can be harnessed or compromised in disease states offers promising strategies for drug development and precision medicine. We invite contributions from diverse fields, including molecular biology, biochemistry, systems biology, and clinical research, to advance the understanding of mitochondrial redox resilience as a cornerstone of cellular health. This journal will serve as a platform for cutting-edge discussions, fostering novel insights into how mitochondria balance redox homeostasis to preserve cellular physiology and mitigate disease.

Prof. Dr. Yuseok Moon
Dr. Ki Hyung Kim
Guest Editors

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Keywords

  • mitochondrial redox
  • mitochondria
  • cellular conditions
  • oxidative damage
  • redox homeostasis
  • cellular aging
  • metabolic disorders
  • cancer
  • inflammation
  • obesity
  • aging
  • mucosal diseases
  • neurodegenerative diseases

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Published Papers (1 paper)

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Research

11 pages, 3393 KiB  
Article
Aryl Hydrocarbon Receptor Is Required for Fasting-Induced Improvement of Gut Barrier Integrity in Caenorhabditis elegans
by Junjie Sun and Yuseok Moon
Antioxidants 2025, 14(8), 905; https://doi.org/10.3390/antiox14080905 - 24 Jul 2025
Viewed by 317
Abstract
The intestinal barrier governs organismal health through nutrient absorption, microbial homeostasis, and immune surveillance. While calorie restriction (CR) enhances metabolic health, the molecular mechanisms underlying its beneficial effects on gut integrity remain unclear. Here, we demonstrate that the aryl hydrocarbon receptor (AHR), a [...] Read more.
The intestinal barrier governs organismal health through nutrient absorption, microbial homeostasis, and immune surveillance. While calorie restriction (CR) enhances metabolic health, the molecular mechanisms underlying its beneficial effects on gut integrity remain unclear. Here, we demonstrate that the aryl hydrocarbon receptor (AHR), a conserved xenobiotic sensor and metabolic regulator, is essential for CR-mediated improvements in intestinal function. Using Caenorhabditis elegans (C. elegans), we subjected wild-type (N2) and AHR-deficient strains (CZ2485 and ZG24) to ad libitum feeding (AL), intermittent fasting (IF), or complete food deprivation (FD). In wild-type animals, intermittent fasting markedly reduced intestinal permeability and bacterial burden while enhancing mitochondrial function and reducing reactive oxygen species. Complete food deprivation conferred modest benefits. Remarkably, these protective effects were severely compromised in AHR mutants, which exhibited increased gut leakage, bacterial colonization, and mitochondrial oxidative stress under fasting conditions. These findings establish AHR as a critical mediator of fasting-induced intestinal resilience, revealing a previously unrecognized regulatory axis linking metabolic sensing to gut barrier homeostasis. Our work illuminates fundamental mechanisms through which calorie restriction promotes gastrointestinal health and identifies AHR-dependent pathways as promising therapeutic targets for metabolic and inflammatory distress affecting the gut–systemic interface. Full article
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