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Cells
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Effects of Microglia Changes on Neuroinflammation and Neurodegeneration
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Effects of Microglia Changes on Neuroinflammation and Neurodegeneration

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 May 2024 | Viewed by 1617

Special Issue Editors

Dr. Chi-Su Yoon

E-Mail Website
Guest Editor
College of Pharmacy, Wonkwang University, Iksan-si, Republic of Korea
Interests: inflammation; neuroinflammation; natural products
Dr. Dong-Sung Lee

E-Mail Website
Guest Editor
College of Pharmacy, Chosun University, Gwangju 61452, Republic of Korea
Interests: natural products; bioactive natural compounds; inflammation; neuroinflammation; neuroprotection; oxidative stress; skin diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Human lifespans have significantly extended, leading to a continuous growth in the percentage of elderly individuals in the population. This has led to the prevalence of numerous neurodegenerative diseases such as dementia, Parkinson’s, Alzheimer’s, and Huntington’s disease. Microglia are found in the Central Nervous System (CNS), and these cells play crucial roles in the regulation of neuroinflammation and neurodegeneration. Neuroinflammation and neurodegeneration are key factors in the genesis of several neurodegenerative diseases; therefore, the importance of microglia research has been recognized, and studies in the related areas have proliferated.

This Special Issue will include (1) mechanism studies of neuroinflammation in microglia; (2) mechanism studies of neurodegeneration in microglia; and (3) studies on therapeutical candidates for microglia during neuroinflammation and neurodegeneration.

Dr. Chi-Su Yoon
Dr. Dong-Sung Lee
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

  • microglia
  • neuroinflammation
  • neurodegenerative disease
  • neurodegeneration
  • central nervous system

Published Papers (1 paper)

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Research

14 pages, 1828 KiB  
Article
Imeglimin Exhibits Novel Anti-Inflammatory Effects on High-Glucose-Stimulated Mouse Microglia through ULK1-Mediated Suppression of the TXNIP–NLRP3 Axis
by Hisashi Kato, Kaori Iwashita, Masayo Iwasa, Sayaka Kato, Hajime Yamakage, Takayoshi Suganami, Masashi Tanaka and Noriko Satoh-Asahara
Cells 2024, 13(3), 284; https://doi.org/10.3390/cells13030284 - 05 Feb 2024
Viewed by 1403
Abstract
Type 2 diabetes mellitus (T2DM) is an epidemiological risk factor for dementia and has been implicated in multifactorial pathologies, including neuroinflammation. In the present study, we aimed to elucidate the potential anti-inflammatory effects of imeglimin, a novel antidiabetic agent, on high-glucose (HG)-stimulated microglia. [...] Read more.
Type 2 diabetes mellitus (T2DM) is an epidemiological risk factor for dementia and has been implicated in multifactorial pathologies, including neuroinflammation. In the present study, we aimed to elucidate the potential anti-inflammatory effects of imeglimin, a novel antidiabetic agent, on high-glucose (HG)-stimulated microglia. Mouse microglial BV2 cells were stimulated with HG in the presence or absence of imeglimin. We examined the effects of imeglimin on the levels of proinflammatory cytokines, intracellular reactive oxygen species (ROS), mitochondrial integrity, and components related to the inflammasome or autophagy pathways in these cells. Our results showed that imeglimin suppressed the HG-induced production of interleukin-1beta (IL-1β) by reducing the intracellular ROS levels, ameliorating mitochondrial dysfunction, and inhibiting the activation of the thioredoxin-interacting protein (TXNIP)–NOD-like receptor family pyrin domain containing 3 (NLRP3) axis. Moreover, the inhibitory effects of imeglimin on the TXNIP–NLRP3 axis depended on the imeglimin-induced activation of ULK1, which also exhibited novel anti-inflammatory effects without autophagy induction. These findings suggest that imeglimin exerted novel suppressive effects on HG-stimulated microglia through the ULK1–TXNIP–NLRP3 axis, and may, thereby, contribute to the development of innovative strategies to prevent T2DM-associated cognitive impairment. Full article
(This article belongs to the Special Issue Effects of Microglia Changes on Neuroinflammation and Neurodegeneration)
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