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Cells
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Cellular Mechanisms Associated with Intermittent Hypoxia
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Cellular Mechanisms Associated with Intermittent Hypoxia

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 October 2024 | Viewed by 6602

Special Issue Editors

Prof. Dr. Asuncion Rocher

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Guest Editor
Department of Biochemistry, Molecular Biology and Physiology, Institute of Molecular Biology and Genetics (IBGM), University of Valladolid-CSIC, Valladolid, Spain
Interests: oxygen sensing; carotid body; chemoreception; signalling pathways; hypoxia; intermittent hypoxia; neurotransmitters; reactive oxygen species; endothelial dysfunction
Special Issues, Collections and Topics in MDPI journals
Dr. Philip I. Aaronson

E-Mail Website
Guest Editor
Department of Inflammation Biology, School of Immunology and Microbial Sciences, King's College London, London, UK
Interests: oxygen sensing; hypoxic pulmonary vasoconstriction; reactive oxygen species; hydrogen sulphide; pulmonary hypertension
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Hypoxia, commonly defined as the reduced availability of oxygen in the tissues produced by different causes (e.g., sleep breathing, pulmonary disorders, anaemia, cardiovascular alterations), plays an important role in the genesis of several human pathologies, including cardiovascular, renal, myocardial, and cerebral diseases in foetal, young, and adult life. Intermittent hypoxia (IH) associated with sleep disordered breathing is one of the major contributing factors in a variety of autonomic abnormalities resulting in hypertension, metabolic syndrome, and stroke. 

Increased reactive oxygen species (ROS) and the ensuing oxidative stress, and the activation of oxygen sensitive transcription factors which induce upregulation of different genes to cope with cellular effects related to a decrease in oxygen levels, are important cellular mechanisms mediating cardiorespiratory and metabolic changes caused by IH in experimental models and in patients with recurrent apnoea.

For this issue, we welcome manuscripts that attempt to unravel the complex molecular and cellular mechanisms involved in the progression of IH-induced alterations, essential to identify new therapeutic targets. 

The Special Issue will cover but is not limited to the following subjects:

  • Oxidative stress, reactive oxygen species, inflammation, and their interplay and impact in the cellular response to intermittent hypoxia;
  • Genomics and transcriptomics insights into the response to intermittent hypoxia;
  • Proteomic and post-translational modifications, signalling pathways, and networks implicated in the response to intermittent hypoxia. 

We will accept original research, reviews, mini-reviews, and perspectives. 

Prof. Dr. Asuncion Rocher
Dr. Philip I. Aaronson
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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
  • reactive oxygen species
  • oxidative stress
  • hypoxia inducible factors
  • inflammation
  • DNA methylation
  • cell signalling
  • transcriptional responses
  • autonomic dysfunction
  • insulin resistance
  • endothelial dysfunction
  • systemic and pulmonary hypertension

Published Papers (3 papers)

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Research

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29 pages, 2931 KiB  
Article
Chronic Intermittent Hypoxia-Induced Diaphragm Muscle Weakness Is NADPH Oxidase-2 Dependent
by Sarah E. Drummond, David P. Burns, Sarah El Maghrani, Oscar Ziegler, Vincent Healy and Ken D. O’Halloran
Cells 2023, 12(14), 1834; https://doi.org/10.3390/cells12141834 - 12 Jul 2023
Viewed by 1306
Abstract
Chronic intermittent hypoxia (CIH)-induced redox alterations underlie diaphragm muscle dysfunction. We sought to establish if NADPH oxidase 2 (NOX2)-derived reactive oxygen species (ROS) underpin CIH-induced changes in diaphragm muscle, which manifest as impaired muscle performance. Adult male mice (C57BL/6J) were assigned to one [...] Read more.
Chronic intermittent hypoxia (CIH)-induced redox alterations underlie diaphragm muscle dysfunction. We sought to establish if NADPH oxidase 2 (NOX2)-derived reactive oxygen species (ROS) underpin CIH-induced changes in diaphragm muscle, which manifest as impaired muscle performance. Adult male mice (C57BL/6J) were assigned to one of three groups: normoxic controls (sham); chronic intermittent hypoxia-exposed (CIH, 12 cycles/hour, 8 h/day for 14 days); and CIH + apocynin (NOX2 inhibitor, 2 mM) administered in the drinking water throughout exposure to CIH. In separate studies, we examined sham and CIH-exposed NOX2-null mice (B6.129S-CybbTM1Din/J). Apocynin co-treatment or NOX2 deletion proved efficacious in entirely preventing diaphragm muscle dysfunction following exposure to CIH. Exposure to CIH had no effect on NOX2 expression. However, NOX4 mRNA expression was increased following exposure to CIH in wild-type and NOX2 null mice. There was no evidence of overt CIH-induced oxidative stress. A NOX2-dependent increase in genes related to muscle regeneration, antioxidant capacity, and autophagy and atrophy was evident following exposure to CIH. We suggest that NOX-dependent CIH-induced diaphragm muscle weakness has the potential to affect ventilatory and non-ventilatory performance of the respiratory system. Therapeutic strategies employing NOX2 blockade may function as an adjunct therapy to improve diaphragm muscle performance and reduce disease burden in diseases characterised by exposure to CIH, such as obstructive sleep apnoea. Full article
(This article belongs to the Special Issue Cellular Mechanisms Associated with Intermittent Hypoxia)
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12 pages, 2888 KiB  
Article
Chronic Intermittent Hypoxia Increases Cell Proliferation in Hepatocellular Carcinoma
by Lydie Carreres, Marion Mercey-Ressejac, Keerthi Kurma, Julien Ghelfi, Carole Fournier, Olivier Manches, Florent Chuffart, Sophie Rousseaux, Mélanie Minoves, Thomas Decaens, Herve Lerat and Zuzana Macek Jilkova
Cells 2022, 11(13), 2051; https://doi.org/10.3390/cells11132051 - 28 Jun 2022
Cited by 7 | Viewed by 2141
Abstract
Obstructive sleep apnea (OSA) syndrome is characterized by chronic intermittent hypoxia and is associated with an increased risk of all-cause mortality, including cancer mortality. Hepatocellular carcinoma (HCC) is the most common type of liver cancer, characterized by increasing incidence and high mortality. However, [...] Read more.
Obstructive sleep apnea (OSA) syndrome is characterized by chronic intermittent hypoxia and is associated with an increased risk of all-cause mortality, including cancer mortality. Hepatocellular carcinoma (HCC) is the most common type of liver cancer, characterized by increasing incidence and high mortality. However, the link between HCC and OSA-related chronic intermittent hypoxia remains unclear. Herein, we used a diethylnitrosamine (DEN)-induced HCC model to investigate whether OSA-related chronic intermittent hypoxia has an impact on HCC progression. To elucidate the associated mechanisms, we first evaluated the hypoxia status in the DEN-induced HCC model. Next, to simulate OSA-related intermittent hypoxia, we exposed cirrhotic rats with HCC to intermittent hypoxia during six weeks. We performed histopathological, immunohistochemical, RT-qPCR, and RNA-seq analysis. Chronic DEN injections strongly promoted cell proliferation, fibrosis, disorganized vasculature, and hypoxia in liver tissue, which mimics the usual events observed during human HCC development. Intermittent hypoxia further increased cell proliferation in DEN-induced HCC, which may contribute to an increased risk of HCC progression. In conclusion, our observations suggest that chronic intermittent hypoxia may be a factor worsening the prognosis of HCC. Full article
(This article belongs to the Special Issue Cellular Mechanisms Associated with Intermittent Hypoxia)
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Review

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12 pages, 703 KiB  
Review
Mechanisms of Atrial Fibrillation in Obstructive Sleep Apnoea
by James Saleeb-Mousa, Demitris Nathanael, Andrew M. Coney, Manish Kalla, Keith L. Brain and Andrew P. Holmes
Cells 2023, 12(12), 1661; https://doi.org/10.3390/cells12121661 - 19 Jun 2023
Cited by 4 | Viewed by 2482
Abstract
Obstructive sleep apnoea (OSA) is a strong independent risk factor for atrial fibrillation (AF). Emerging clinical data cite adverse effects of OSA on AF induction, maintenance, disease severity, and responsiveness to treatment. Prevention using continuous positive airway pressure (CPAP) is effective in some [...] Read more.
Obstructive sleep apnoea (OSA) is a strong independent risk factor for atrial fibrillation (AF). Emerging clinical data cite adverse effects of OSA on AF induction, maintenance, disease severity, and responsiveness to treatment. Prevention using continuous positive airway pressure (CPAP) is effective in some groups but is limited by its poor compliance. Thus, an improved understanding of the underlying arrhythmogenic mechanisms will facilitate the development of novel therapies and/or better selection of those currently available to complement CPAP in alleviating the burden of AF in OSA. Arrhythmogenesis in OSA is a multifactorial process characterised by a combination of acute atrial stimulation on a background of chronic electrical, structural, and autonomic remodelling. Chronic intermittent hypoxia (CIH), a key feature of OSA, is associated with long-term adaptive changes in myocyte ion channel currents, sensitising the atria to episodic bursts of autonomic reflex activity. CIH is also a potent driver of inflammatory and hypoxic stress, leading to fibrosis, connexin downregulation, and conduction slowing. Atrial stretch is brought about by negative thoracic pressure (NTP) swings during apnoea, promoting further chronic structural remodelling, as well as acutely dysregulating calcium handling and electrical function. Here, we provide an up-to-date review of these topical mechanistic insights and their roles in arrhythmia. Full article
(This article belongs to the Special Issue Cellular Mechanisms Associated with Intermittent Hypoxia)
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