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Antioxidants
Special Issues
Redox Enzymes in Neurodegenerative Diseases
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Redox Enzymes in Neurodegenerative Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Antioxidant Enzyme Systems".

Deadline for manuscript submissions: closed (28 February 2021) | Viewed by 7169

Special Issue Editor

Dr. Dong-Hoon Hyun

E-Mail Website
Guest Editor
Department of Life Science, College of Natural Sciences, Ewha Womans University, Seoul 03760, Republic of Korea
Interests: oxidative stress; aging intervention; plasma membrane redox enzymes; mitochondrial bioenergetics; abnormal protein handling

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) are produced mainly in the mitochondria and are required for cells to proliferate and survive through ROS-dependent signalling pathways under normal physiological conditions. However, an imbalance between the production and elimination of ROS causes oxidative damage to biomolecules and mitochondrial dysfunction and is closely associated with a variety of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. The brain is particularly vulnerable to oxidative stress due to high oxygen consumption, high contents of unsaturated fatty acids and relatively low levels of antioxidant defence. Understanding the mechanisms of redox homeostasis and energy metabolism in the brain can help delay or prevent the progression of neurodegenerative diseases.

The purpose of this Special Issue is to bring together latest research involved in the activities of antioxidant enzymes and the regulation of redox homeostasis in healthy and pathological conditions. Molecular mechanism studies using in vitro and/or in vivo systems aimed at cellular stress responses can be included in this Special Issue. In addition, approaches to the regulation of redox enzymes in brain diseases, through neurohormetic phytochemicals, dietary restriction and exercise, will also be considered.

Dr. Dong-Hoon Hyun
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

  • oxidative stress
  • antioxidants
  • mitochondrial dysfunction
  • brain metabolism
  • redox enzymes
  • neurohormesis
  • Alzheimer’s disease
  • Parkinson’s disease
  • amyotrophic lateral sclerosis

Published Papers (2 papers)

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Research

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16 pages, 6108 KiB  
Article
Nucleoredoxin Knockdown in SH-SY5Y Cells Promotes Cell Renewal
by Lucie Valek and Irmgard Tegeder
Antioxidants 2021, 10(3), 449; https://doi.org/10.3390/antiox10030449 - 13 Mar 2021
Cited by 4 | Viewed by 2949
Abstract
Nucleoredoxin (NXN) is a redox regulator of Disheveled and thereby of WNT signaling. Deficiency in mice leads to cranial dysmorphisms and defects of heart, brain, and bone, suggesting defects of cell fate determination. We used shRNA-mediated knockdown of NXN in SH-SY5Y neuroblastoma cells [...] Read more.
Nucleoredoxin (NXN) is a redox regulator of Disheveled and thereby of WNT signaling. Deficiency in mice leads to cranial dysmorphisms and defects of heart, brain, and bone, suggesting defects of cell fate determination. We used shRNA-mediated knockdown of NXN in SH-SY5Y neuroblastoma cells to study its impact on neuronal cells. We expected that shNXN cells would easily succumb to redox stress, but there were no differences in viability on stimulation with hydrogen peroxide. Instead, the proliferation of naïve shNXN cells was increased with a higher rate of mitotic cells in cell cycle analyses. In addition, basal respiratory rates were higher, whereas the relative change in oxygen consumption upon mitochondrial stressors was similar to control cells. shNXN cells had an increased expression of redox-sensitive heat shock proteins, Hsc70/HSPA8 and HSP90, and autophagy markers suggested an increase in autophagosome formation upon stimulation with bafilomycin and higher flux under low dose rapamycin. A high rate of self-renewal, autophagy, and upregulation of redox-sensitive chaperones appears to be an attractive anti-aging combination if it were to occur in neurons in vivo for which SH-SY5Y cells are a model. Full article
(This article belongs to the Special Issue Redox Enzymes in Neurodegenerative Diseases)
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Review

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16 pages, 1666 KiB  
Review
Intersection between Redox Homeostasis and Autophagy: Valuable Insights into Neurodegeneration
by Hyungsun Park, Jongyoon Kim, Chihoon Shin and Seongju Lee
Antioxidants 2021, 10(5), 694; https://doi.org/10.3390/antiox10050694 - 28 Apr 2021
Cited by 19 | Viewed by 3406
Abstract
Autophagy, a main degradation pathway for maintaining cellular homeostasis, and redox homeostasis have recently been considered to play protective roles in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Increased levels of reactive oxygen species (ROS) in neurons can [...] Read more.
Autophagy, a main degradation pathway for maintaining cellular homeostasis, and redox homeostasis have recently been considered to play protective roles in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Increased levels of reactive oxygen species (ROS) in neurons can induce mitochondrial damage and protein aggregation, thereby resulting in neurodegeneration. Oxidative stress is one of the major activation signals for the induction of autophagy. Upon activation, autophagy can remove ROS, damaged mitochondria, and aggregated proteins from the cells. Thus, autophagy can be an effective strategy to maintain redox homeostasis in the brain. However, the interaction between redox homeostasis and autophagy is not clearly elucidated. In this review, we discuss recent studies on the relationship between redox homeostasis and autophagy associated with neurodegenerative diseases and propose that autophagy induction through pharmacological intervention or genetic activation might be a promising strategy to treat these disorders. Full article
(This article belongs to the Special Issue Redox Enzymes in Neurodegenerative Diseases)
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