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Antioxidants
Special Issues
Trace Elements, Redox Balance, and Neurological Diseases
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Trace Elements, Redox Balance, and Neurological Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 31 May 2025 | Viewed by 955

Special Issue Editors

Prof. Dr. Yan-Zhong Chang

E-Mail Website
Guest Editor
Laboratory of Molecular Iron Metabolism, College of Life Science, Hebei Normal University, Shijiazhuang 050024, China
Interests: iron metabolism; iron misregulation; redox imbalance; Parkinson's disease; Alzheimer's disease; stroke; mental and emotional disorders; preparation and safety evaluation of brain-targeted nanomedicines
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Hong Jiang

E-Mail Website
Guest Editor
School of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao, China
Interests: neurodegenerative diseases; Parkinson’s disease; α-synuclein; iron metabolism; proteostasis; ghrelin

Special Issue Information

Dear Colleagues,

Trace elements are indispensable for organisms to execute normal physiological functions. In recent years, breakthroughs have been achieved in the exploration of the following areas: imbalanced trace element metabolism has a significant impact on the onset of neurological diseases; the intricate signaling pathways that initiate redox imbalance are closely related to trace elements; oxidation-reduction imbalance plays an important role in the genesis and progression of neurological diseases and the aging process. Therefore, the demand to focus on showcasing recent advances in these areas is becoming increasingly strong.

This Special Issue aims to explore the latest progress made in terms of the effects of trace elements such as iron, copper, zinc, selenium, manganese, etc., on neurodevelopment, aging, psychological disorders, and neurological diseases, including stroke, Parkinson's disease, Alzheimer's disease, Huntington's disease, ALS, etc., and to explore the mechanisms of cell division, differentiation, migration, aging, apoptosis, ferroptosis, and necrosis related to the regulation of redox signaling caused by an imbalance in trace element metabolism.

This Special Issue will present new advances in research in this field, promoting further development of the study of trace elements, redox balance, and neurological diseases.

Prof. Dr. Yan-Zhong Chang
Prof. Dr. Hong Jiang
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. 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

  • iron
  • copper
  • zinc
  • selenium
  • redox
  • Alzheimer's disease
  • Parkinson's disease
  • stroke
  • ageing
  • brain-targeted nanomedicines

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Published Papers (1 paper)

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Research

15 pages, 5096 KiB  
Article
Downregulation of Iron–Sulfur Cluster Biogenesis May Contribute to Hyperglycemia-Mediated Diabetic Peripheral Neuropathy in Murine Models
by Lin Wu, Fei Huang, Zichen Sun, Jinghua Zhang, Siyu Xia, Hongting Zhao, Yutong Liu, Lu Yang, Yibing Ding, Dezhi Bian, Kuanyu Li and Yu Sun
Antioxidants 2024, 13(9), 1036; https://doi.org/10.3390/antiox13091036 - 26 Aug 2024
Viewed by 740
Abstract
Background: Diabetic peripheral neuropathy (DPN) is considered one of the most common chronic complications of diabetes. Impairment of mitochondrial function is regarded as one of the causes. Iron–sulfur clusters are essential cofactors for numerous iron–sulfur (Fe-S)-containing proteins/enzymes, including mitochondrial electron transport chain complex [...] Read more.
Background: Diabetic peripheral neuropathy (DPN) is considered one of the most common chronic complications of diabetes. Impairment of mitochondrial function is regarded as one of the causes. Iron–sulfur clusters are essential cofactors for numerous iron–sulfur (Fe-S)-containing proteins/enzymes, including mitochondrial electron transport chain complex I, II, and III and aconitase. Methods: To determine the impact of hyperglycemia on peripheral nerves, we used Schwann-like RSC96 cells and classical db/db mice to detect the expression of Fe-S-related proteins, mitochondrially enzymatic activities, and iron metabolism. Subsequently, we treated high-glucose-induced RSC96 cells and db/db mice with pioglitazone (PGZ), respectively, to evaluate the effects on Fe-S cluster biogenesis, mitochondrial function, and animal behavior. Results: We found that the core components of Fe-S biogenesis machinery, such as frataxin (Fxn) and scaffold protein IscU, significantly decreased in high-glucose-induced RSC96 cells and db/db mice, accompanied by compromised mitochondrial Fe-S-containing enzymatic activities, such as complex I and II and aconitase. Consequently, oxidative stress and inflammation increased. PGZ not only has antidiabetic effects but also increases the expression of Fxn and IscU to enhance mitochondrial function in RSC96 cells and db/db mice. Meanwhile, PGZ significantly alleviated sciatic nerve injury and improved peripheral neuronal behavior, accompanied by suppressed oxidative stress and inflammation in the sciatic nerve of the db/db mice. Conclusions: Iron–sulfur cluster deficiency may contribute to hyperglycemia-mediated DPN. Full article
(This article belongs to the Special Issue Trace Elements, Redox Balance, and Neurological Diseases)
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