Ferroptosis: Can Iron be the Last or Cure for a Cell?

Asuman Akkaya Fırat
{"title":"Ferroptosis: Can Iron be the Last or Cure for a Cell?","authors":"Asuman Akkaya Fırat","doi":"10.5772/intechopen.101426","DOIUrl":null,"url":null,"abstract":"Ferroptosis is one of the forms of programmed cell death. Besides being a necessary micronutrient, iron is the key element that initiates ferroptosis in the cell. Intracellular unstable iron accumulation increases the amount of intracellular ROS, especially by the peroxidation of unsaturated membrane phospholipids. Insufficient antioxidant capacity and decreased glutathione levels play an important role in this process. The research reveals that an imbalance between unoxidized polyunsaturated fatty acids (PUFAs) and oxidized PUFAs, particularly oxidized arachidonic acid, accelerates ferroptosis. These oxidative reactions change the permeability of lysosomal and cellular membranes and cell death occurs. Iron chelators, lipophilic antioxidants, and specific inhibitors prevent ferroptosis. In addition to being accepted as a physiological process, it seems to be associated with tissue reperfusion damage, ischemic, neurodegenerative diseases, hematological and nephrological disorders. Ferroptosis is also being explored as a treatment option where it may offer a treatment option for some types of cancer. In this section, the brief history of ferroptosis, its morphological, molecular, and pathophysiological features are mentioned. Ferroptosis seems to be a rich field of research as a treatment option for many diseases in the future.","PeriodicalId":14524,"journal":{"name":"Iron Metabolism - Iron a Double‐Edged Sword [Working Title]","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2021-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Iron Metabolism - Iron a Double‐Edged Sword [Working Title]","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5772/intechopen.101426","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Ferroptosis is one of the forms of programmed cell death. Besides being a necessary micronutrient, iron is the key element that initiates ferroptosis in the cell. Intracellular unstable iron accumulation increases the amount of intracellular ROS, especially by the peroxidation of unsaturated membrane phospholipids. Insufficient antioxidant capacity and decreased glutathione levels play an important role in this process. The research reveals that an imbalance between unoxidized polyunsaturated fatty acids (PUFAs) and oxidized PUFAs, particularly oxidized arachidonic acid, accelerates ferroptosis. These oxidative reactions change the permeability of lysosomal and cellular membranes and cell death occurs. Iron chelators, lipophilic antioxidants, and specific inhibitors prevent ferroptosis. In addition to being accepted as a physiological process, it seems to be associated with tissue reperfusion damage, ischemic, neurodegenerative diseases, hematological and nephrological disorders. Ferroptosis is also being explored as a treatment option where it may offer a treatment option for some types of cancer. In this section, the brief history of ferroptosis, its morphological, molecular, and pathophysiological features are mentioned. Ferroptosis seems to be a rich field of research as a treatment option for many diseases in the future.
铁下垂:铁是细胞的最后或治愈方法吗?
铁下垂是程序性细胞死亡的一种形式。除了作为一种必需的微量营养素外,铁是细胞中启动铁下垂的关键元素。细胞内不稳定的铁积累增加了细胞内ROS的数量,特别是通过不饱和膜磷脂的过氧化作用。抗氧化能力不足和谷胱甘肽水平降低在这一过程中起重要作用。研究表明,未氧化多不饱和脂肪酸(PUFAs)和氧化多不饱和脂肪酸(PUFAs)之间的不平衡,特别是氧化花生四烯酸,加速了铁下垂。这些氧化反应改变溶酶体和细胞膜的通透性,导致细胞死亡。铁螯合剂、亲脂性抗氧化剂和特异性抑制剂可预防铁下垂。除了被认为是一个生理过程外,它似乎与组织再灌注损伤、缺血性、神经退行性疾病、血液和肾脏疾病有关。上睑下垂也正在被探索作为一种治疗选择,它可能为某些类型的癌症提供治疗选择。在这一节,铁下垂的简史,其形态学,分子和病理生理特征被提及。作为未来许多疾病的治疗选择,上睑下垂似乎是一个丰富的研究领域。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信