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Ferroptosis: Emerging Mechanisms, Physiological Functions, and Therapeutic Applications
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Ferroptosis: Emerging Mechanisms, Physiological Functions, and Therapeutic Applications

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 20 June 2025 | Viewed by 2584

Special Issue Editor

Dr. Shibiao Wan

E-Mail Website
Guest Editor
Department of Genetics, Cell Biology and Anatomy, College of Medicine, University of Nebraska Medical Center, Omaha, NE 68198, USA
Interests: bioinformatics; machine learning; computational biology; genomics; cancer research; single cell analysis; multi-omics analysis; spatial transcriptomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ferroptosis is a form of programmed cell death that is triggered by the accumulation of intracellular lipid peroxidation and is dependent on iron. Recent studies have shown that ferroptosis plays a crucial role in regulating cell oxidative stress, metabolism, and immune response, and is involved in various physiological and pathological processes in the body. It is now understood that ferroptosis can inhibit tumor growth and enhance the effectiveness of chemotherapy and immunotherapy in treating cancer. However, ferroptosis can also lead to damage in normal tissues and organs, contributing to the development of diseases such as cardiovascular and neurodegenerative disorders. By targeting ferroptosis and understanding its role in disease progression, researchers can develop new strategies for treatment and potentially improve human health outcomes.

In this Special Issue, we invite submissions of perspective, original article, review, commentary, or letter type of manuscripts that delve into topics such as, but not limited to, the following:

  1. ferroptosis and disease occurrence and/or development;
  2. ferroptosis biomarkers for lipid and/or iron metabolism in the onset and progression of diseases;
  3. Gene regulation of ferroptosis in diseases;
  4. Development and application of ferroptosis inhibitors and agonists (including nanomaterials);
  5. Application of ferroptosis in precision medicine and clinical transformation.

Dr. Shibiao Wan
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • biomarker
  • iron metabolism
  • diseases
  • precision medicine

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Published Papers (2 papers)

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18 pages, 1482 KiB  
Article
Jacaric Acid Empowers RSL3-Induced Ferroptotic Cell Death in Two- and Three-Dimensional Breast Cancer Cell Models
by Géraldine Cuvelier, Perrine Vermonden, Pauline Debisschop, Manon Martin, Françoise Derouane, Gerhard Liebisch, Josef Ecker, Marcus Hoering, Martine Berlière, Mieke Van Bockstal, Christine Galant, François Duhoux, Larissa Mourao, Colinda Scheele, Olivier Feron, René Rezsohazy, Cyril Corbet and Yvan Larondelle
Int. J. Mol. Sci. 2025, 26(7), 3375; https://doi.org/10.3390/ijms26073375 - 4 Apr 2025
Viewed by 67
Abstract
Ferroptosis has recently emerged as a promising strategy to combat therapy-resistant cancers. As lipid peroxidation is a key trigger of ferroptotic cell death, enhancing cancer cell susceptibility through the supply of highly peroxidisable fatty acids represents a novel therapeutic approach. Conjugated linolenic acids [...] Read more.
Ferroptosis has recently emerged as a promising strategy to combat therapy-resistant cancers. As lipid peroxidation is a key trigger of ferroptotic cell death, enhancing cancer cell susceptibility through the supply of highly peroxidisable fatty acids represents a novel therapeutic approach. Conjugated linolenic acids (CLnAs) fulfill this requirement, exhibiting a peroxidation propagation rate eight times higher than their non-conjugated counterpart, α-linolenic acid. This study evaluates jacaric acid (JA), a plant-derived CLnA, as a ferroptotic inducer, both as a monotherapy and in combination with RAS-selective lethal 3 (RSL3), a canonical ferroptosis inducer, in 2D and 3D breast cancer cell models. JA treatment significantly reduced cell viability across all models, primarily through lipid peroxidation driven by JA incorporation into cellular lipids rather than alterations in anti-ferroptotic gene expression. Moreover, JA synergistically enhanced RSL3 cytotoxicity under 2D and several 3D conditions. Similar effects were observed with punicic acid, another plant-derived CLnA isomer. Our study exploits a common feature of cancer metabolism, increased fatty acid uptake, to turn it into a vulnerability. The incorporation of JA into breast cancer cells creates a highly peroxidisable environment that increases cancer cell sensitivity to RSL3, potentially reducing required doses and minimising side effects. Full article
(This article belongs to the Special Issue Ferroptosis: Emerging Mechanisms, Physiological Functions, and Therapeutic Applications)
26 pages, 6695 KiB  
Article
A Systems Biology Approach Towards a Comprehensive Understanding of Ferroptosis
by Mikhail Arbatskiy, Dmitriy Balandin, Ilya Akberdin and Alexey Churov
Int. J. Mol. Sci. 2024, 25(21), 11782; https://doi.org/10.3390/ijms252111782 - 2 Nov 2024
Viewed by 1747
Abstract
Ferroptosis is a regulated cell death process characterized by iron ion catalysis and reactive oxygen species, leading to lipid peroxidation. This mechanism plays a crucial role in age-related diseases, including cancer and cardiovascular and neurological disorders. To better mimic iron-induced cell death, predict [...] Read more.
Ferroptosis is a regulated cell death process characterized by iron ion catalysis and reactive oxygen species, leading to lipid peroxidation. This mechanism plays a crucial role in age-related diseases, including cancer and cardiovascular and neurological disorders. To better mimic iron-induced cell death, predict the effects of various elements, and identify drugs capable of regulating ferroptosis, it is essential to develop precise models of this process. Such drugs can be tested on cellular models. Systems biology offers a powerful approach to studying biological processes through modeling, which involves accumulating and analyzing comprehensive research data. Once a model is created, it allows for examining the system’s response to various stimuli. Our goal is to develop a modular framework for ferroptosis, enabling the prediction and screening of compounds with geroprotective and antiferroptotic effects. For modeling and analysis, we utilized BioUML (Biological Universal Modeling Language), which supports key standards in systems biology, modular and visual modeling, rapid simulation, parameter estimation, and a variety of numerical methods. This combination fulfills the requirements for modeling complex biological systems. The integrated modular model was validated on diverse datasets, including original experimental data. This framework encompasses essential molecular genetic processes such as the Fenton reaction, iron metabolism, lipid synthesis, and the antioxidant system. We identified structural relationships between molecular agents within each module and compared them to our proposed system for regulating the initiation and progression of ferroptosis. Our research highlights that no current models comprehensively cover all regulatory mechanisms of ferroptosis. By integrating data on ferroptosis modules into an integrated modular model, we can enhance our understanding of its mechanisms and assist in the discovery of new treatment targets for age-related diseases. A computational model of ferroptosis was developed based on a modular modeling approach and included 73 differential equations and 93 species. Full article
(This article belongs to the Special Issue Ferroptosis: Emerging Mechanisms, Physiological Functions, and Therapeutic Applications)
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