Autophagy: Restoration of Cells and Tissues

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

Deadline for manuscript submissions: closed (1 December 2022) | Viewed by 2783

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Guest Editor
Department of Biochemistry and Genetics, Zhejiang University School of Medicine, Hangzhou, China
Interests: autophagy; organelle-interaction network
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Special Issue Information

Dear Colleagues,

Macroautophagy (hereafter referred to as autophagy) is a lysosomal degradative pathway, which plays a fundamental role in cellular, tissue, and organismal homeostasis. The deregulation of autophagy is tightly associated with a variety of human diseases, especially neurodegenerative, inflammatory disorders and cancer.

This special issue is expected to examine how autophagy selectively targets damaged organelles, invading microbes, and toxic protein aggregates, to summarize how the deficiencies in abovementioned processes may lead to different types of human diseases, and to discuss how to design novel therapeutics to potentially reverse the pathogenesis of human disease and ageing caused by dysfunctional autophagy.

Prof. Dr. Qiming Sun 
Guest Editor

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Keywords

  • macroautophagy
  • homeostasis
  • dysfunctional autophagy
  • neurodegenerative diseases
  • cancer

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Published Papers (1 paper)

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Research

17 pages, 3442 KiB  
Article
Sleep-Disturbance-Induced Microglial Activation Involves CRH-Mediated Galectin 3 and Autophagy Dysregulation
by Liyang Guo, Kirstin M. Reed, Ashley Carter, Yan Cheng, Soheil Kazemi Roodsari, Damian Martinez Pineda, Laurie L. Wellman, Larry D. Sanford and Ming-Lei Guo
Cells 2023, 12(1), 160; https://doi.org/10.3390/cells12010160 - 30 Dec 2022
Cited by 5 | Viewed by 2307
Abstract
Chronic sleep disturbances (CSDs) including insomnia, insufficient sleep time, and poor sleep quality are major public health concerns around the world, especially in developed countries. CSDs are major health risk factors linked to multiple neurodegenerative and neuropsychological diseases. It has been suggested that [...] Read more.
Chronic sleep disturbances (CSDs) including insomnia, insufficient sleep time, and poor sleep quality are major public health concerns around the world, especially in developed countries. CSDs are major health risk factors linked to multiple neurodegenerative and neuropsychological diseases. It has been suggested that CSDs could activate microglia (Mg) leading to increased neuroinflammation levels, which ultimately lead to neuronal dysfunction. However, the detailed mechanisms underlying CSD-mediated microglial activation remain mostly unexplored. In this study, we used mice with three-weeks of sleep fragmentation (SF) to explore the underlying pathways responsible for Mg activation. Our results revealed that SF activates Mg in the hippocampus (HP) but not in the striatum and prefrontal cortex (PFc). SF increased the levels of corticotropin-releasing hormone (CRH) in the HP. In vitro mechanism studies revealed that CRH activation of Mg involves galectin 3 (Gal3) upregulation and autophagy dysregulation. CRH could disrupt lysosome membrane integrity resulting in lysosomal cathepsins leakage. CRHR2 blockage mitigated CRH-mediated effects on microglia in vitro. SF mice also show increased Gal3 levels and autophagy dysregulation in the HP compared to controls. Taken together, our results show that SF-mediated hippocampal Mg activation involves CRH mediated galectin 3 and autophagy dysregulation. These findings suggest that targeting the hippocampal CRH system might be a novel therapeutic approach to ameliorate CSD-mediated neuroinflammation and neurodegenerative diseases. Full article
(This article belongs to the Special Issue Autophagy: Restoration of Cells and Tissues)
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