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Cells
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Molecular and Cellular Basis of Sleep Disorders
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Molecular and Cellular Basis of Sleep Disorders

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

Deadline for manuscript submissions: 25 December 2024 | Viewed by 2120

Special Issue Editor

Dr. Dae-Wui Yoon

E-Mail Website
Guest Editor
Department of Biomedical Laboratory Science, Jungwon University, 85, Munmu-ro, Goesan-eup, Goesan-gun, Chungbuk 28204, Republic of Korea
Interests: sleep fragmentation; epigenetics; cancer; proteomics; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Obstructive sleep apnea (OSA) is a very common sleep disorder. OSA is characterized by repeated obstruction of the upper airway during sleep, accompanied by intermittent hypoxia, sleep fragmentation, and fluctuations of intra-negative pressure. OSA is an independent risk factor of a variety of chronic diseases and dysfunctions, such as cardiovascular disease, metabolic disease, and neurocognitive dysfunction. Several molecular and cellular mechanisms involving inflammation and oxidative stress have been proposed to cause the development of OSA and OSA-related diseases, but the exact mechanisms remain elusive.

In this Special Issue, we will discuss recent interesting findings from in vitro studies; animal models including intermittent hypoxia, sleep fragmentation, and sleep deprivation; and human biomarker studies that provide insights into the pathogenesis of OSA and OSA-related diseases from a molecular and cellular perspective. These topics will ultimately allow us to develop therapeutic strategies for the treatment of OSA and OSA comorbidities.  

Dr. Dae-Wui Yoon
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. 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
  • sleep fragmentation
  • sleep deprivation
  • OSA animal model
  • biomarkers

Published Papers (2 papers)

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Research

23 pages, 5532 KiB  
Article
Chronic Astrocytic TNFα Production in the Preoptic-Basal Forebrain Causes Aging-like Sleep–Wake Disturbances in Young Mice
by Andrey Kostin, Md. Aftab Alam, Anton Saevskiy and Md. Noor Alam
Cells 2024, 13(11), 894; https://doi.org/10.3390/cells13110894 - 22 May 2024
Viewed by 691
Abstract
Sleep disruption is a frequent problem of advancing age, often accompanied by low-grade chronic central and peripheral inflammation. We examined whether chronic neuroinflammation in the preoptic and basal forebrain area (POA-BF), a critical sleep–wake regulatory structure, contributes to this disruption. We developed a [...] Read more.
Sleep disruption is a frequent problem of advancing age, often accompanied by low-grade chronic central and peripheral inflammation. We examined whether chronic neuroinflammation in the preoptic and basal forebrain area (POA-BF), a critical sleep–wake regulatory structure, contributes to this disruption. We developed a targeted viral vector designed to overexpress tumor necrosis factor-alpha (TNFα), specifically in astrocytes (AAV5-GFAP-TNFα-mCherry), and injected it into the POA of young mice to induce heightened neuroinflammation within the POA-BF. Compared to the control (treated with AAV5-GFAP-mCherry), mice with astrocytic TNFα overproduction within the POA-BF exhibited signs of increased microglia activation, indicating a heightened local inflammatory milieu. These mice also exhibited aging-like changes in sleep–wake organization and physical performance, including (a) impaired sleep–wake functions characterized by disruptions in sleep and waking during light and dark phases, respectively, and a reduced ability to compensate for sleep loss; (b) dysfunctional VLPO sleep-active neurons, indicated by fewer neurons expressing c-fos after suvorexant-induced sleep; and (c) compromised physical performance as demonstrated by a decline in grip strength. These findings suggest that inflammation-induced dysfunction of sleep- and wake-regulatory mechanisms within the POA-BF may be a critical component of sleep–wake disturbances in aging. Full article
(This article belongs to the Special Issue Molecular and Cellular Basis of Sleep Disorders)
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13 pages, 4335 KiB  
Article
Melatonin Improves Glucose Homeostasis and Insulin Sensitivity by Mitigating Inflammation and Activating AMPK Signaling in a Mouse Model of Sleep Fragmentation
by Seok Hyun Hong, Da-Been Lee, Dae-Wui Yoon and Jinkwan Kim
Cells 2024, 13(6), 470; https://doi.org/10.3390/cells13060470 - 7 Mar 2024
Viewed by 1131
Abstract
Sleep fragmentation (SF) can increase inflammation and production of reactive oxygen species (ROS), leading to metabolic dysfunction. SF is associated with inflammation of adipose tissue and insulin resistance. Several studies have suggested that melatonin may have beneficial metabolic effects due to activating AMP-activated [...] Read more.
Sleep fragmentation (SF) can increase inflammation and production of reactive oxygen species (ROS), leading to metabolic dysfunction. SF is associated with inflammation of adipose tissue and insulin resistance. Several studies have suggested that melatonin may have beneficial metabolic effects due to activating AMP-activated protein kinase (AMPK). However, it is unclear whether melatonin affects the AMPK signaling pathway in SF-induced metabolic dysfunction. Therefore, we hypothesize that SF induces metabolic impairment and inflammation in white adipose tissue (WAT), as well as altered intracellular homeostasis. We further hypothesize that these conditions could be improved by melatonin treatment. We conducted an experiment using adult male C57BL/6 mice, which were divided into three groups: control, SF, and SF with melatonin treatment (SF+Mel). The SF mice were housed in SF chambers, while the SF+Mel mice received daily oral melatonin. After 12 weeks, glucose tolerance tests, insulin tolerance tests, adipose tissue inflammation tests, and AMPK assessments were performed. The SF mice showed increased weight gain, impaired glucose regulation, inflammation, and decreased AMPK in WAT compared to the controls. Melatonin significantly improved these outcomes by mitigating SF-induced metabolic dysfunction, inflammation, and AMPK downregulation in adipose tissue. The therapeutic efficacy of melatonin against cardiometabolic impairments in SF may be due to its ability to restore adipose tissue homeostatic pathways. Full article
(This article belongs to the Special Issue Molecular and Cellular Basis of Sleep Disorders)
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