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Antioxidants
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Oxidative Stress and Sleep Disorders
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Oxidative Stress and 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: closed (15 October 2022) | Viewed by 9405

Special Issue Editor

Prof. Dr. Elise Belaïdi

E-Mail Website
Guest Editor
Laboratoire HP2, Grenoble Alpes University, INSERM, CHU Grenoble Alpes, 38000 Grenoble, France
Interests: intermittent hypoxia; hypoxia inducible factor-1; myocardial ischemia-reperfusion, metabolism, signaling mathway

Special Issue Information

Dear Colleagues,

Sleep apnea syndrome (SAS) is a worldwide pathology strongly associated with cardiovascular diseases, such as ischemic heart diseases (i.e., myocardial infarction, ischemic heart failure), heart failure, hypertension, and stroke. It is also associated with metabolic pathologies such as obesity and type 2 diabetes. One of the major consequence of SAS is chronic intermittent hypoxia which is now well recognized to generate oxidative stress. Oxidative stress plays an important role in cardiovascular and metabolic pathologies development and progression. Interestingly, oxidative stress exerts an ambivalent role; it is involved in physiological processes in order to adapt the organism to its environment but it is also involved in pathophysiological processes, such as ichemia-reperfusion injury, metabolism alterations, and, SAS-associated cardiovascular and metabolic diseases. Therefore, the specific mechanisms involved in oxidative stress generation, as well as the underlying mechanism of oxidative stress, represent a particularly great interest in order to deeply understand how oxidative stress induces beneficial and deleterious responses, in the context of intermittent hypoxia which is also an ambivalent stimulus. Thus, studies aim at determining or characterizing beneficial or deleterious oxidative stress will lead to open new insights in managing oxidative stress and, consequently, in maintaining redox homeostasis and organ function, particularly in the context of SAS. 

This Special Issue (SI) particularly focuses on: 

  • oxidative stress generates by intermittent hypoxia;
  • intermittent hypoxia-induced oxidative stress and underlying mechanisms;
  • intermittent hypoxia-associated mechanisms linked to oxidative stress; 
  • antioxidant strategies to counteract SAS/IH-associated pathologies. 

All scientific works (original research papers, perspectives, hypotheses, opinions, reviews, modelling approaches, and methods) in this field are deeply welcome.

Prof. Dr. Elise Belaïdi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind 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

  • intermittent hypoxia
  • cardiovascular diseases
  • metabolic diseases
  • oxidative stress

Published Papers (4 papers)

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Research

14 pages, 2150 KiB  
Article
CaMKII-Dependent Contractile Dysfunction and Pro-Arrhythmic Activity in a Mouse Model of Obstructive Sleep Apnea
by Philipp Hegner, Simon Lebek, Benedikt Schaner, Florian Ofner, Mathias Gugg, Lars Siegfried Maier, Michael Arzt and Stefan Wagner
Antioxidants 2023, 12(2), 315; https://doi.org/10.3390/antiox12020315 - 29 Jan 2023
Cited by 2 | Viewed by 1413
Abstract
Left ventricular contractile dysfunction and arrhythmias frequently occur in patients with sleep-disordered breathing (SDB). The CaMKII-dependent dysregulation of cellular Ca homeostasis has recently been described in SDB patients, but these studies only partly explain the mechanism and are limited by the patients’ heterogeneity. [...] Read more.
Left ventricular contractile dysfunction and arrhythmias frequently occur in patients with sleep-disordered breathing (SDB). The CaMKII-dependent dysregulation of cellular Ca homeostasis has recently been described in SDB patients, but these studies only partly explain the mechanism and are limited by the patients’ heterogeneity. Here, we analyzed contractile function and Ca homeostasis in a mouse model of obstructive sleep apnea (OSA) that is not limited by confounding comorbidities. OSA was induced by artificial tongue enlargement with polytetrafluorethylene (PTFE) injection into the tongue of wildtype mice and mice with a genetic ablation of the oxidative activation sites of CaMKII (MMVV knock-in). After eight weeks, cardiac function was assessed with echocardiography. Reactive oxygen species (ROS) and Ca transients were measured using confocal and epifluorescence microscopy, respectively. Wildtype PTFE mice exhibited an impaired ejection fraction, while MMVV PTFE mice were fully protected. As expected, isolated cardiomyocytes from PTFE mice showed increased ROS production. We further observed decreased levels of steady-state Ca transients, decreased levels of caffeine-induced Ca transients, and increased pro-arrhythmic activity (defined as deviations from the diastolic Ca baseline) only in wildtype but not in MMVV PTFE mice. In summary, in the absence of any comorbidities, OSA was associated with contractile dysfunction and pro-arrhythmic activity and the inhibition of the oxidative activation of CaMKII conveyed cardioprotection, which may have therapeutic implications. Full article
(This article belongs to the Special Issue Oxidative Stress and Sleep Disorders)
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16 pages, 2560 KiB  
Article
L-Citrulline Supplementation Reduces Blood Pressure and Myocardial Infarct Size under Chronic Intermittent Hypoxia, a Major Feature of Sleep Apnea Syndrome
by Bilgehan Ozcan, Britanny Blachot-Minassian, Stéphanie Paradis, Lucile Mazière, Marie Chambion-Diaz, Sophie Bouyon, Jean-Louis Pépin, Vincent Pialoux, Claire Arnaud, Christophe Moinard and Elise Belaidi
Antioxidants 2022, 11(12), 2326; https://doi.org/10.3390/antiox11122326 - 24 Nov 2022
Cited by 3 | Viewed by 3106
Abstract
Intermittent hypoxia (IH) is a landmark of obstructive sleep apnea (OSA) at the core of the cardiovascular consequences of OSA. IH triggers oxidative stress, a major underlying mechanism for elevated blood pressure (BP) and increased infarct size. L-citrulline is an amino acid that [...] Read more.
Intermittent hypoxia (IH) is a landmark of obstructive sleep apnea (OSA) at the core of the cardiovascular consequences of OSA. IH triggers oxidative stress, a major underlying mechanism for elevated blood pressure (BP) and increased infarct size. L-citrulline is an amino acid that has been demonstrated to be protective of the cardiovascular system and exert pleiotropic effects. Therefore, we tested the impact of citrulline supplementation on IH-induced increase in BP and infarct size. Four groups of rats exposed to normoxia (N) or IH [14 days (d), 8 h/day, 30 s-O2 21%/30 s-O2 5%] and were supplemented or not with citrulline (1 g·kg−1·d−1). After 14 d, BP was measured, and hearts were submitted to global ischemia-reperfusion to measure infarct size. Histological and biochemical analyses were conducted on hearts and aorta to assess oxidative stress. Citrulline significantly reduced BP (–9.92%) and infarct size (–18.22%) under IH only. In the aorta, citrulline supplementation significantly decreased superoxide anion and nitrotyrosine levels under IH and abolished the IH-induced decrease in nitrite. Citrulline supplementation significantly decreased myocardial superoxide anion levels and xanthine oxidase enzyme activity under IH. Citrulline shows a cardioprotective capacity by limiting IH-induced pro-oxidant activity. Our results suggest that citrulline might represent a new pharmacological strategy in OSA patients with high cardiovascular risk. Full article
(This article belongs to the Special Issue Oxidative Stress and Sleep Disorders)
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17 pages, 2824 KiB  
Article
Comprehensive Metabolomics and Machine Learning Identify Profound Oxidative Stress and Inflammation Signatures in Hypertensive Patients with Obstructive Sleep Apnea
by Zhiyong Du, Haili Sun, Yunhui Du, Linyi Li, Qianwen Lv, Huahui Yu, Fan Li, Yu Wang, Xiaolu Jiao, Chaowei Hu and Yanwen Qin
Antioxidants 2022, 11(10), 1946; https://doi.org/10.3390/antiox11101946 - 29 Sep 2022
Cited by 4 | Viewed by 1833
Abstract
Obstructive sleep apnea (OSA) can aggravate blood pressure and increase the risk of cardiovascular diseases in hypertensive individuals, yet the underlying pathophysiological process is still incompletely understood. More importantly, OSA remains a significantly undiagnosed condition. In this study, a total of 559 hypertensive [...] Read more.
Obstructive sleep apnea (OSA) can aggravate blood pressure and increase the risk of cardiovascular diseases in hypertensive individuals, yet the underlying pathophysiological process is still incompletely understood. More importantly, OSA remains a significantly undiagnosed condition. In this study, a total of 559 hypertensive patients with and without OSA were included. Metabolome and lipidome-wide analyses were performed to explore the pathophysiological processes of hypertension comorbid OSA and derive potential biomarkers for diagnosing OSA in hypertensive subjects. Compared to non-OSA hypertensive patients (discovery set = 120; validation set = 116), patients with OSA (discovery set = 165; validation set = 158) demonstrated a unique sera metabolic phenotype dominated by abnormalities in biological processes of oxidative stress and inflammation. By integrating three machine learning algorithms, six discriminatory metabolites (including 5-hydroxyeicosatetraenoic acid, taurine, histidine, lysophosphatidic acid 16:0, lysophosphatidylcholine 18:0, and dihydrosphingosine) were selected for constructing diagnostic and classified model. Notably, the established multivariate-model could accurately identify OSA subjects. The corresponding area under the curve values and the correct classification rates were 0.995 and 96.8% for discovery sets, 0.997 and 99.1% for validation sets. This work updates the molecular insights of hypertension comorbid OSA and paves the way for the use of metabolomics for the diagnosis of OSA in hypertensive individuals. Full article
(This article belongs to the Special Issue Oxidative Stress and Sleep Disorders)
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17 pages, 2939 KiB  
Article
Intermittent Hypoxia-Induced Cardiomyocyte Death Is Mediated by HIF-1 Dependent MAM Disruption
by Sophie Moulin, Amandine Thomas, Stefan Wagner, Michael Arzt, Hervé Dubouchaud, Frédéric Lamarche, Sophie Bouyon, Guillaume Vial, Diane Godin-Ribuot, Jean-Louis Pépin, Claire Arnaud and Elise Belaidi
Antioxidants 2022, 11(8), 1462; https://doi.org/10.3390/antiox11081462 - 27 Jul 2022
Cited by 9 | Viewed by 2260
Abstract
Rationale: Intermittent hypoxia (IH) is one of the main features of sleep-disordered breathing (SDB). Recent findings indicate that hypoxia inducible factor-1 (HIF-1) promotes cardiomyocytes apoptosis during chronic IH, but the mechanisms involved remain to be elucidated. Here, we hypothesize that IH-induced ER stress [...] Read more.
Rationale: Intermittent hypoxia (IH) is one of the main features of sleep-disordered breathing (SDB). Recent findings indicate that hypoxia inducible factor-1 (HIF-1) promotes cardiomyocytes apoptosis during chronic IH, but the mechanisms involved remain to be elucidated. Here, we hypothesize that IH-induced ER stress is associated with mitochondria-associated ER membrane (MAM) alteration and mitochondrial dysfunction, through HIF-1 activation. Methods: Right atrial appendage biopsies from patients with and without SDB were used to determine HIF-1α, Grp78 and CHOP expressions. Wild-type and HIF-1α+/− mice were exposed to normoxia (N) or IH (21–5% O2, 60 cycles/h, 8 h/day) for 21 days. Expressions of HIF-1α, Grp78 and CHOP, and apoptosis, were measured by Western blot and immunochemistry. In isolated cardiomyocytes, we examined structural integrity of MAM by proximity ligation assay and their function by measuring ER-to-mitochondria Ca2+ transfer by confocal microscopy. Finally, we measured mitochondrial respiration using oxygraphy and calcium retention capacity (CRC) by spectrofluorometry. MAM structure was also investigated in H9C2 cells incubated with 1 mM CoCl2, a potent HIF-1α inducer. Results: In human atrial biopsies and mice, IH induced HIF-1 activation, ER stress and apoptosis. IH disrupted MAM, altered Ca2+ homeostasis, mitochondrial respiration and CRC. Importantly, IH had no effect in HIF-1α+/− mice. Similar to what observed under IH, HIF-1α overexpression was associated with MAM alteration in H9C2. Conclusion: IH-induced ER stress, MAM alterations and mitochondrial dysfunction were mediated by HIF-1; all these intermediate mechanisms ultimately inducing cardiomyocyte apoptosis. This suggests that HIF-1 modulation might limit the deleterious cardiac effects of SDB. Full article
(This article belongs to the Special Issue Oxidative Stress and Sleep Disorders)
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