Mitochondrial and Redox Signaling in Exercise, Aging, and Metabolic Health

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: 31 December 2026 | Viewed by 837

Editors


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Guest Editor
Animal and Human Physiology Department, Faculty of Biology, University of Gdansk, Gdansk, Poland
Interests: metabolic in physical exercise and training; nutrition supplements; reactive oxygen
Special Issues, Collections and Topics in MDPI journals

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Guest Editor Assistant
Animal and Human Physiology Department, Faculty of Biology, University of Gdansk, Gdansk, Poland
Interests: musculoskeletal physiotherapy; stress response; antioxidant activity

Special Issue Information

Dear Colleagues,

Maintaining redox homeostasis and mitochondrial function is essential for cellular plasticity, physical performance, and healthy aging. The balance between redox signaling and mitochondrial metabolism regulates physiological adaptations to exercise, nutritional status, and metabolic or environmental challenges. When these regulatory pathways are disturbed, the risk of sarcopenia, metabolic dysfunction, osteoporosis, and other age-related or neurodegenerative diseases increases substantially.

This Special Issue aims to highlight the integrative role of redox and mitochondrial pathways as molecular regulators connecting exercise, metabolic function, and neuromuscular health across the lifespan.

We welcome original research and review articles addressing molecular, cellular, and translational aspects of redox biology in the context of exercise, aging, neurodegeneration, and metabolic regulation.

We encourage submissions from researchers working at the intersection of molecular biology, physiology, and clinical research.

Topics of interest include, but are not limited to, the following:

  • Redox signaling and mitochondrial regulation in exercise adaptation, fatigue, and neuroprotection;
  • Mitochondrial biogenesis and quality control in aging skeletal muscle and brain;
  • Exercise-induced modulation of antioxidant defenses, neurotrophic signaling, and metabolic health;
  • Redox control of myokine, osteokine, and neurotrophic factor activity;
  • Vitamin D-dependent regulation of redox balance in muscle, bone, and neuro-metabolic crosstalk;
  • Oxidative stress, inflammation, and mitochondrial dysfunction in sarcopenia, osteoporosis, and neurodegenerative diseases;
  • Nutritional and pharmacological interventions targeting mitochondrial and redox pathways in the regulation of the muscle–brain axis;
  • Redox biomarkers and translational perspectives in exercise, aging, and neurodegenerative diseases.

Dr. Jan Jacek Kaczor
Guest Editor

Dr. Mateusz Jakub Karnia
Guest Editor Assistant

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly 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 2900 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
  • skeletal muscle
  • exercise
  • aging
  • metabolism
  • oxidative stress
  • muscle–brain crosstalk
  • sarcopenia
  • osteoporosis
  • neurodegenerative diseases

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Published Papers (1 paper)

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Research

23 pages, 3304 KB  
Article
Translational Insights into Exercise-Induced Protective Adaptations in 5XFAD Mice and Middle-Aged Amateur Sportsmen
by Pau Garcia-Baucells, Clara Bartra, Sara Sarroca, Filipa Reinoite, Júlia Senserrich, Rubén Corpas, Christian Griñán-Ferré and Coral Sanfeliu
Antioxidants 2026, 15(6), 698; https://doi.org/10.3390/antiox15060698 - 31 May 2026
Viewed by 424
Abstract
The increase in antioxidant defenses mediated by physical exercise signaling is proposed to be a protective factor against brain aging and neurodegeneration. However, the processes involved, particularly the response of senescence markers and cell fitness status in the context of Alzheimer’s disease (AD) [...] Read more.
The increase in antioxidant defenses mediated by physical exercise signaling is proposed to be a protective factor against brain aging and neurodegeneration. However, the processes involved, particularly the response of senescence markers and cell fitness status in the context of Alzheimer’s disease (AD) pathology, remain unclear. We analyzed male and female 5XFAD transgenic AD mice subjected to 6 months of voluntary wheel running using molecular and behavioral techniques. Levels of mRNA of selected genes, mitochondrial complex proteins, and proteasomal function, were analyzed in the cerebral cortex or hippocampus. In an exploratory translational approach, proteasomal dynamics- and senescence-related genes were analyzed in peripheral blood from middle-aged amateur sportsmen. Physical exercise increased expression of antioxidant genes and modulated epigenetic genes in 5XFAD male and female mice. An increase in protein levels of hippocampal mitochondrial complexes CIII and CV was also induced in males. Both exercised 5XFAD mice and veteran sportsmen showed improved proteasomal status and decreased expression of senescence genes. Exercised mice showed memory and behavior preservation, as well as increases in brain metabolic fitness and gene modulation. These changes may contribute to the neuroprotective effect of physical exercise. Full article
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