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Ferroptosis: Mechanisms and Human Disease
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Ferroptosis: Mechanisms and Human Disease

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1130

Special Issue Editor

Dr. Chan-Yen Kuo

E-Mail Website
Guest Editor
Department of Research, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City 23142, Taiwan
Interests: oxidant stress; DNA damage and repair; microenvironment and tumorigenesis; nature products; inflammation and cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ferroptosis is a unique form of cell death, driven by iron-dependent phospholipid peroxidation, which is regulated by a wide range of cellular metabolic processes, including redox homeostasis, iron handling, mitochondrial activity, amino acid, lipid, and sugar metabolism, in addition to several signaling pathways that are relevant to diseases. It is important to note that ferroptosis is closely associated with many diseases on a pathological level. It is also important to note that ferroptosis is closely associated with many diseases on a pathological level. In recent years, research has focused on regulating ferroptosis to prevent and treat diseases associated with it. The presence of ferroptosis is currently found in numerous common diseases such as tumors, inflammatory diseases, bacterial infections, pulmonary fibrosis, hepatitis, inflammatory bowel diseases, neurodegenerative diseases, kidney damage, ischemic-reperfusion damage, skeletal muscle damage, and neurodegenerative diseases. Authors are encouraged to discuss the characteristics and mechanisms of ferroptosis in this Special Issue and summarize how ferroptosis plays a role in pathophysiological processes in a wide variety of systemic diseases, which may serve as new references for treating clinical diseases.

Dr. Chan-Yen Kuo
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. Biology 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 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

  • ferroptosis
  • systemic diseases
  • inflammatory response
  • mitochondrial-dependent redox homeostasis
  • microenvironment

Published Papers (1 paper)

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Research

17 pages, 4231 KiB  
Article
Increased Vulnerability to Ferroptosis in FUS-ALS
by Muhammad Ismail, Dajana Großmann and Andreas Hermann
Biology 2024, 13(4), 215; https://doi.org/10.3390/biology13040215 - 26 Mar 2024
Viewed by 769
Abstract
Ferroptosis, a regulated form of cell death characterized by iron-dependent lipid peroxide accumulation, plays a pivotal role in various pathological conditions, including neurodegenerative diseases. While reasonable evidence for ferroptosis exists, e.g., in Parkinson’s disease or Alzheimer’s disease, there are only a few reports [...] Read more.
Ferroptosis, a regulated form of cell death characterized by iron-dependent lipid peroxide accumulation, plays a pivotal role in various pathological conditions, including neurodegenerative diseases. While reasonable evidence for ferroptosis exists, e.g., in Parkinson’s disease or Alzheimer’s disease, there are only a few reports on amyotrophic lateral sclerosis (ALS), a fast progressive and incurable neurodegenerative disease characterized by progressive motor neuron degeneration. Interestingly, initial studies have suggested that ferroptosis might be significantly involved in ALS. Key features of ferroptosis include oxidative stress, glutathione depletion, and alterations in mitochondrial morphology and function, mediated by proteins such as GPX4, xCT, ACSL4 FSP1, Nrf2, and TfR1. Induction of ferroptosis involves small molecule compounds like erastin and RSL3, which disrupt system Xc− and GPX4 activity, respectively, resulting in lipid peroxidation and cellular demise. Mutations in fused in sarcoma (FUS) are associated with familial ALS. Pathophysiological hallmarks of FUS-ALS involve mitochondrial dysfunction and oxidative damage, implicating ferroptosis as a putative cell-death pathway in motor neuron demise. However, a mechanistic understanding of ferroptosis in ALS, particularly FUS-ALS, remains limited. Here, we investigated the vulnerability to ferroptosis in FUS-ALS cell models, revealing mitochondrial disturbances and increased susceptibility to ferroptosis in cells harboring ALS-causing FUS mutations. This was accompanied by an altered expression of ferroptosis-associated proteins, particularly by a reduction in xCT expression, leading to cellular imbalance in the redox system and increased lipid peroxidation. Iron chelation with deferoxamine, as well as inhibition of the mitochondrial calcium uniporter (MCU), significantly alleviated ferroptotic cell death and lipid peroxidation. These findings suggest a link between ferroptosis and FUS-ALS, offering potential new therapeutic targets. Full article
(This article belongs to the Special Issue Ferroptosis: Mechanisms and Human Disease)
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