Oxidative Stress in Sleep Disorders

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: 25 March 2026 | Viewed by 1010

Special Issue Editor

Special Issue Information

Dear Colleagues,

Sleep disorders affect a significant portion of the global population. Conditions like insomnia, sleep apnea, and restless leg syndrome are linked to various physiological disruptions. One of the most significant mechanisms involved in the development and exacerbation of sleep disorders is oxidative stress.

Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body's ability to neutralize them with antioxidants. This imbalance can lead to cellular damage, inflammation, and the deterioration of normal biological functions. In sleep disorders, disruptions to sleep patterns and reduced sleep quality have been shown to increase oxidative damage, which can further impair sleep quality in a cyclical manner.

This Special Issue delves into recent research on the relationship between oxidative stress and sleep disturbances. It explores the role of oxidative stress in various sleep disorders, the potential mechanisms involved, and the implications for treatment. It also highlights emerging therapeutic strategies, such as antioxidant interventions, that aim to alleviate the harmful effects of oxidative stress and improve sleep quality, offering new avenues for clinical practice and future research in the field.

Dr. Agata Gabryelska
Guest Editor

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Keywords

  • sleep disorders
  • sleep apnea
  • insomnia
  • oxidative stress

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Published Papers (1 paper)

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Research

18 pages, 2350 KB  
Article
Normalization of Oxygen Levels Induces a Metabolic Reprogramming in Livers Exposed to Intermittent Hypoxia Mimicking Obstructive Sleep Apnea
by Miguel Á. Hernández-García, Beatriz Aldave-Orzáiz, Carlos Ernesto Fernández-García, Esther Fuertes-Yebra, Esther Rey, Ángela Berlana, Ramón Farré, Carmelo García-Monzón, Isaac Almendros, Pedro Landete and Águeda González-Rodríguez
Antioxidants 2025, 14(8), 971; https://doi.org/10.3390/antiox14080971 - 7 Aug 2025
Viewed by 674
Abstract
Obstructive sleep apnea (OSA), characterized by intermittent hypoxia (IH), is strongly associated with metabolic syndrome and metabolic dysfunction-associated steatotic liver disease (MASLD). IH exacerbates MASLD progression through oxidative stress, inflammation, and lipid accumulation. This study aims to investigate the impact of oxygen normalization [...] Read more.
Obstructive sleep apnea (OSA), characterized by intermittent hypoxia (IH), is strongly associated with metabolic syndrome and metabolic dysfunction-associated steatotic liver disease (MASLD). IH exacerbates MASLD progression through oxidative stress, inflammation, and lipid accumulation. This study aims to investigate the impact of oxygen normalization on metabolic dysfunction in OSA patients using continuous positive airway pressure (CPAP) therapy, and in mice exposed to IH followed by a reoxygenation period. In the clinical study, 76 participants (44 OSA patients and 32 controls) were analyzed. OSA patients had higher insulin resistance, triglycerides, very low density lipoprotein (VLDL) content, and liver enzyme levels, along with a higher prevalence of liver steatosis. After 18 months of CPAP therapy, OSA patients showed significant improvements in insulin resistance, lipid profiles (total cholesterol and VLDL), liver function markers (AST and albumin), and steatosis risk scores (Fatty Liver Index and OWLiver test). In the experimental study, IH induced hepatic lipid accumulation, oxidative stress, and inflammation, and reoxygenation reversed these deleterious effects in mice. At the molecular level, IH downregulated fatty acid oxidation (FAO)-related genes, thus impairing the FAO process. Reoxygenation maintained elevated levels of lipogenic genes but restored FAO gene expression and activity, suggesting enhanced lipid clearance despite ongoing lipogenesis. Indeed, serum β hydroxybutyrate, a key marker of hepatic FAO in patients, was impaired in OSA patients but normalized after CPAP therapy, supporting improved FAO function. CPAP therapy improves lipid profiles, liver function, and MASLD progression in OSA patients. Experimental findings highlight the therapeutic potential of oxygen normalization in reversing IH-induced liver damage by FAO pathway restoration, indicating a metabolic reprogramming in the liver. Full article
(This article belongs to the Special Issue Oxidative Stress in Sleep Disorders)
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