Ferroptosis induced by environmental pollutants and its health implications.

IF 6.1 2区 生物学 Q1 CELL BIOLOGY Cell Death Discovery Pub Date : 2025-01-24 DOI:10.1038/s41420-025-02305-2
Fu-Han Gong, Liyuan Liu, Xuesheng Wang, Qi Xiang, Xin Yi, Ding-Sheng Jiang
{"title":"Ferroptosis induced by environmental pollutants and its health implications.","authors":"Fu-Han Gong, Liyuan Liu, Xuesheng Wang, Qi Xiang, Xin Yi, Ding-Sheng Jiang","doi":"10.1038/s41420-025-02305-2","DOIUrl":null,"url":null,"abstract":"<p><p>Environmental pollution represents a significant public health concern, with the potential health risks associated with environmental pollutants receiving considerable attention over an extended period. In recent years, a substantial body of research has been dedicated to this topic. Since the discovery of ferroptosis, an iron-dependent programmed cell death typically characterized by lipid peroxidation, in 2012, there have been significant advances in the study of its role and mechanism in various diseases. A growing number of recent studies have also demonstrated the involvement of ferroptosis in the damage caused to the organism by environmental pollutants, and the molecular mechanisms involved have been partially elucidated. The targeting of ferroptosis has been demonstrated to be an effective means of ameliorating the health damage caused by PM2.5, organic and inorganic pollutants, and ionizing radiation. This review begins by providing a summary of the most recent and important advances in ferroptosis. It then proceeds to offer a critical analysis of the health effects and molecular mechanisms of ferroptosis induced by various environmental pollutants. Furthermore, as is the case with all rapidly evolving research areas, there are numerous unanswered questions and challenges pertaining to environmental pollutant-induced ferroptosis, which we discuss in this review in an attempt to provide some directions and clues for future research in this field.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"20"},"PeriodicalIF":6.1000,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759704/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Death Discovery","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41420-025-02305-2","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Environmental pollution represents a significant public health concern, with the potential health risks associated with environmental pollutants receiving considerable attention over an extended period. In recent years, a substantial body of research has been dedicated to this topic. Since the discovery of ferroptosis, an iron-dependent programmed cell death typically characterized by lipid peroxidation, in 2012, there have been significant advances in the study of its role and mechanism in various diseases. A growing number of recent studies have also demonstrated the involvement of ferroptosis in the damage caused to the organism by environmental pollutants, and the molecular mechanisms involved have been partially elucidated. The targeting of ferroptosis has been demonstrated to be an effective means of ameliorating the health damage caused by PM2.5, organic and inorganic pollutants, and ionizing radiation. This review begins by providing a summary of the most recent and important advances in ferroptosis. It then proceeds to offer a critical analysis of the health effects and molecular mechanisms of ferroptosis induced by various environmental pollutants. Furthermore, as is the case with all rapidly evolving research areas, there are numerous unanswered questions and challenges pertaining to environmental pollutant-induced ferroptosis, which we discuss in this review in an attempt to provide some directions and clues for future research in this field.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
求助全文
约1分钟内获得全文 去求助
来源期刊
Cell Death Discovery
Cell Death Discovery Biochemistry, Genetics and Molecular Biology-Cell Biology
CiteScore
8.30
自引率
1.40%
发文量
468
审稿时长
9 weeks
期刊介绍: Cell Death Discovery is a multidisciplinary, international, online-only, open access journal, dedicated to publishing research at the intersection of medicine with biochemistry, pharmacology, immunology, cell biology and cell death, provided it is scientifically sound. The unrestricted access to research findings in Cell Death Discovery will foster a dynamic and highly productive dialogue between basic scientists and clinicians, as well as researchers in industry with a focus on cancer, neurobiology and inflammation research. As an official journal of the Cell Death Differentiation Association (ADMC), Cell Death Discovery will build upon the success of Cell Death & Differentiation and Cell Death & Disease in publishing important peer-reviewed original research, timely reviews and editorial commentary. Cell Death Discovery is committed to increasing the reproducibility of research. To this end, in conjunction with its sister journals Cell Death & Differentiation and Cell Death & Disease, Cell Death Discovery provides a unique forum for scientists as well as clinicians and members of the pharmaceutical and biotechnical industry. It is committed to the rapid publication of high quality original papers that relate to these subjects, together with topical, usually solicited, reviews, editorial correspondence and occasional commentaries on controversial and scientifically informative issues.
期刊最新文献
Ex.50.T aptamer impairs tumor-stroma cross-talk in breast cancer by targeting gremlin-1. Correction: A Y178C rhodopsin mutation causes aggregation and comparatively severe retinal degeneration. Cell death in tumor microenvironment: an insight for exploiting novel therapeutic approaches. Thyroid hormones inhibit tumor progression and enhance the antitumor activity of lenvatinib in hepatocellular carcinoma via reprogramming glucose metabolism. Mitochondrial priming and response to BH3 mimetics in "one-two punch" senogenic-senolytic strategies.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1