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Antioxidants
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Ferroptosis and Its Potential Role in the Physiopathology of Neurodegenerative...
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Ferroptosis and Its Potential Role in the Physiopathology of Neurodegenerative Disorders

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: 20 October 2024 | Viewed by 833

Special Issue Editor

Dr. Chengliang Luo

E-Mail Website
Guest Editor
Department of Forensic Medicine, School of Basic Medicine and Biological Sciences, Soochow University, Suzhou 215123, China
Interests: brain injury; traumatic brain injury; cognitive function; ferroptosis; cell death; mitochondrion; oxidative stress; neuroinflammation; forensic pathology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ferroptosis, as a novel mode of regulated cell death, is considered a significant mechanism involved in neuroinflammation within the nervous system. Current studies show that ferroptosis and neuroinflammation have a strong spatial and temporal correlation in brain injury, suggesting that the pathophysiological relationship between the two may play an indispensable role in the progression of neurodegenerative disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), anxiety, depression, stroke, and traumatic brain injury (TBI). We invite you to submit your latest original research findings or review articles to this Special Issue, which will bring together current research concerning the molecular mechanisms and potential roles of ferroptosis in the physiopathology of neurodegenerative disorders. Submissions can include both in vitro and in vivo studies relating to, but not limited to, any of the following topics: activation/inhibition mechanism of molecular mediators of ferroptosis after brain injury; modulation of signaling pathways of ferroptosis in neurodegenerative disorders; modulation of molecular mediators of ferroptosis in brain injury; molecular mechanism of signaling pathway of ferroptosis in neuroinflammation progression regulation; and the potential roles of ferroptosis and neuroinflammation in cognitive dysfunction caused by neurodegenerative disorders.

We look forward to your contributions.

Dr. Chengliang Luo
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

  • ferroptosis
  • blood–brain barrier
  • neurodegenerative disorders
  • cognitive dysfunction
  • neuroinflammation

Published Papers (1 paper)

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Review

31 pages, 1342 KiB  
Review
The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders
by Yejia Xu, Bowen Jia, Jing Li, Qianqian Li and Chengliang Luo
Antioxidants 2024, 13(4), 395; https://doi.org/10.3390/antiox13040395 - 26 Mar 2024
Viewed by 678
Abstract
Central neurological disorders are significant contributors to morbidity, mortality, and long-term disability globally in modern society. These encompass neurodegenerative diseases, ischemic brain diseases, traumatic brain injury, epilepsy, depression, and more. The involved pathogenesis is notably intricate and diverse. Ferroptosis and neuroinflammation play pivotal [...] Read more.
Central neurological disorders are significant contributors to morbidity, mortality, and long-term disability globally in modern society. These encompass neurodegenerative diseases, ischemic brain diseases, traumatic brain injury, epilepsy, depression, and more. The involved pathogenesis is notably intricate and diverse. Ferroptosis and neuroinflammation play pivotal roles in elucidating the causes of cognitive impairment stemming from these diseases. Given the concurrent occurrence of ferroptosis and neuroinflammation due to metabolic shifts such as iron and ROS, as well as their critical roles in central nervous disorders, the investigation into the co-regulatory mechanism of ferroptosis and neuroinflammation has emerged as a prominent area of research. This paper delves into the mechanisms of ferroptosis and neuroinflammation in central nervous disorders, along with their interrelationship. It specifically emphasizes the core molecules within the shared pathways governing ferroptosis and neuroinflammation, including SIRT1, Nrf2, NF-κB, Cox-2, iNOS/NO·, and how different immune cells and structures contribute to cognitive dysfunction through these mechanisms. Researchers’ findings suggest that ferroptosis and neuroinflammation mutually promote each other and may represent key factors in the progression of central neurological disorders. A deeper comprehension of the common pathway between cellular ferroptosis and neuroinflammation holds promise for improving symptoms and prognosis related to central neurological disorders. Full article
(This article belongs to the Special Issue Ferroptosis and Its Potential Role in the Physiopathology of Neurodegenerative Disorders)
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