Welcome to Ferroptosis and Oxidative Stress (FOS), a newly established journal dedicated to disseminating high-quality research in the field of cell death, with particular emphasis on responses to oxidative stress. This journal publishes studies on ferroptosis, other forms of regulated cell death, and cellular responses to altered oxidative conditions.
Ferroptosis is a distinct form of cell death, differing from apoptosis, necroptosis, and pyroptosis[1]. It occurs when membrane lipids are converted into lipid peroxides, leading to destabilization of essential cellular membranes. This process is typically initiated by the iron-dependent Fenton reaction (hence the term “ferroptosis”) and proceeds when cellular mechanisms that prevent lipid peroxidation or detoxify lipid peroxides are impaired by cytotoxic drugs, metabolic perturbations, or other stressors.
The need for a dedicated journal arises from the rapid expansion of ferroptosis research. Novel antioxidant pathways continue to be identified[2-5], and new mechanisms through which ferroptosis is engaged are increasingly reported[6-9]. Currently, relevant publications are widely dispersed across multiple journals, potentially slowing the dissemination of important findings. By providing a centralized platform, FOS aims to accelerate communication and foster progress in this emerging field.
A brief introduction is warranted. I have been engaged in research on regulated cell death for nearly forty years, initially focusing on apoptosis and subsequently on necroptosis and pyroptosis. I consider cell death a fundamental biological process, as central to life as cell replication, differentiation, locomotion, and metabolism[10]. While I am not a leading expert in ferroptosis or oxidative stress, I have assembled an exceptional editorial board of recognized leaders in these areas. As Editor-in-Chief, I maintain a position independent of specific approaches, models, or interpretations, focusing solely on the rigor of the data. This perspective is intended to promote unbiased discussion and scientific discourse.
FOS is an open-access journal. During my tenure, no publication fees will be charged. Manuscripts will first undergo editorial assessment for relevance and novelty, followed by rigorous peer review to ensure scientific quality. Authors can expect a fair and transparent review process.
Recognizing the challenges of modern peer review, where extensive revisions and additional experimentation are often required, FOS emphasizes two primary criteria:
1. Do the conclusions advance the field?
2. Are the conclusions fully supported by the data?
Additional experiments suggested by reviewers will be considered optional unless essential for validating the conclusions. Final decisions will also consider overall scientific quality and clarity, reflecting our commitment to a fair and balanced review process.
We warmly welcome you to Ferroptosis and Oxidative Stress and look forward to your contributions to this exciting and rapidly evolving field.
Douglas R. Green
Editor-in-Chief
Authors contribution
The author contributed solely to the article.
Conflicts of interest
Douglas R. Green is the Editor-in-Chief of Ferroptosis and Oxidative Stress. No other conflicts of interest to declare.
Ethical approval
Not applicable.
Consent to participate
Not applicable.
Consent for publication
Not applicable.
Availability of data and materials
Not applicable.
Funding
None.
Copyright
© The Author(s) 2025.
References
-
1. Dixon SJ, Lemberg KM, Lamprecht MR, Skouta R, Zaitsev EM, Gleason CE, et al. Ferroptosis: an iron-dependent form of nonapoptotic cell death. Cell. 2012;149(5):1060-1072.[DOI]
-
2. Bersuker K, Hendricks JM, Li Z, Magtanong L, Ford B, Tang PH, et al. The CoQ oxidoreductase FSP1 acts parallel to GPX4 to inhibit ferroptosis. Nature. 2019;575(7784):688-692.[DOI]
-
3. Mishima E, Ito J, Wu Z, Nakamura T, Wahida A, Doll S, et al. A non-canonical vitamin K cycle is a potent ferroptosis suppressor. Nature. 2022;608(7924):778-783.[DOI]
-
4. Liang D, Feng Y, Zandkarimi F, Wang H, Zhang Z, Kim J, et al. Ferroptosis surveillance independent of GPX4 and differentially regulated by sex hormones. Cell. 2023;186(13):2748-2764.[DOI]
-
5. Nakamura T, Hipp C, Santos Dias Mourão A, Borggräfe J, Aldrovandi M, Henkelmann B, et al. Phase separation of FSP1 promotes ferroptosis. Nature. 2023;619(7969):371-377.[DOI]
-
6. Oh M, Jang SY, Lee JY, Kim JW, Jung Y, Kim J, et al. The lipoprotein-associated phospholipase A2 inhibitor Darapladib sensitises cancer cells to ferroptosis by remodelling lipid metabolism. Nat Commun. 2023;14(1):5728.[DOI]
-
7. Co HK, Wu CC, Lee YC, Chen SH. Emergence of large-scale cell death through ferroptotic trigger waves. Nature. 2024;631(8021):654-662.[DOI]
-
8. Roeck BF, Lotfipour Nasudivar S, Vorndran MR, Schueller L, Yapici FI, Rübsam M, et al. Ferroptosis spreads to neighboring cells via plasma membrane contacts. Nat Commun. 2025;16(1):2951.[DOI]
-
9. Tonnus W, Maremonti F, Gavali S, Schlecht MN, Gembardt F, Belavgeni A et al. Multiple oestradiol functions inhibit ferroptosis and acute kidney injury. Nature. 2025.[DOI]
-
10. Green DR. Cell Death: Apoptosis and other means to an end. 2nd ed. NY: Cold Spring Harbor Press; 2018.
Copyright
© The Author(s) 2025. This is an Open Access article licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
Publisher’s Note
Share And Cite
Science Exploration Style

Science Exploration Style
