The Role of Iron in Atherosclerosis and its Association with Related Diseases.

IF 5.7 2区 医学 Q1 PERIPHERAL VASCULAR DISEASE Current Atherosclerosis Reports Pub Date : 2024-11-09 DOI:10.1007/s11883-024-01251-1
Yingbo Gao, Boda Wang, Mengrui Hu, Yuhan Ma, Bin Zheng
{"title":"The Role of Iron in Atherosclerosis and its Association with Related Diseases.","authors":"Yingbo Gao, Boda Wang, Mengrui Hu, Yuhan Ma, Bin Zheng","doi":"10.1007/s11883-024-01251-1","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose of review: </strong>This review aims to elucidate the multifaceted role of iron in the pathogenesis of atherosclerosis. The primary objective is to summarize recent advances in understanding how iron contributes to atherosclerosis through various cellular mechanisms. Additionally, the review explores the therapeutic implications of targeting iron metabolism in the prevention and treatment of cardiovascular diseases.</p><p><strong>Recent findings: </strong>A growing body of literature suggests that excess iron accelerates the progression of atherosclerosis, with the deleterious form of iron, non-transferrin-bound iron (NTBI), particularly exacerbating this process. Furthermore, iron overload has been demonstrated to play a pivotal role in endothelial cells, vascular smooth muscle cells, and macrophages, contributing to plaque instability and disease progression by promoting lipid peroxidation, oxidative stress, inflammatory responses, and ferroptosis. Iron plays a complex role in atherosclerosis, influencing multiple cellular processes and promoting disease progression. By promoting oxidative stress, inflammation, and ferroptosis, iron exacerbates endothelial dysfunction, smooth muscle cell calcification, and the formation of macrophage-derived foam cells. Targeted therapies focusing on iron metabolism have proven effective in treating atherosclerosis and other cardiovascular diseases.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"27 1","pages":"1"},"PeriodicalIF":5.7000,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Atherosclerosis Reports","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s11883-024-01251-1","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
引用次数: 0

Abstract

Purpose of review: This review aims to elucidate the multifaceted role of iron in the pathogenesis of atherosclerosis. The primary objective is to summarize recent advances in understanding how iron contributes to atherosclerosis through various cellular mechanisms. Additionally, the review explores the therapeutic implications of targeting iron metabolism in the prevention and treatment of cardiovascular diseases.

Recent findings: A growing body of literature suggests that excess iron accelerates the progression of atherosclerosis, with the deleterious form of iron, non-transferrin-bound iron (NTBI), particularly exacerbating this process. Furthermore, iron overload has been demonstrated to play a pivotal role in endothelial cells, vascular smooth muscle cells, and macrophages, contributing to plaque instability and disease progression by promoting lipid peroxidation, oxidative stress, inflammatory responses, and ferroptosis. Iron plays a complex role in atherosclerosis, influencing multiple cellular processes and promoting disease progression. By promoting oxidative stress, inflammation, and ferroptosis, iron exacerbates endothelial dysfunction, smooth muscle cell calcification, and the formation of macrophage-derived foam cells. Targeted therapies focusing on iron metabolism have proven effective in treating atherosclerosis and other cardiovascular diseases.

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
铁在动脉粥样硬化中的作用及其与相关疾病的联系。
综述的目的:本综述旨在阐明铁在动脉粥样硬化发病机制中的多方面作用。主要目的是总结最近在了解铁如何通过各种细胞机制导致动脉粥样硬化方面取得的进展。此外,该综述还探讨了针对铁代谢预防和治疗心血管疾病的治疗意义:越来越多的文献表明,过量的铁会加速动脉粥样硬化的发展,其中有害的铁形式--非转铁蛋白结合铁(NTBI)尤其会加剧这一过程。此外,铁超载已被证明在内皮细胞、血管平滑肌细胞和巨噬细胞中起着关键作用,通过促进脂质过氧化、氧化应激、炎症反应和铁变态反应,导致斑块不稳定和疾病进展。铁在动脉粥样硬化中起着复杂的作用,影响多个细胞过程并促进疾病进展。通过促进氧化应激、炎症反应和铁变态反应,铁加剧了内皮功能障碍、平滑肌细胞钙化和巨噬细胞衍生泡沫细胞的形成。事实证明,针对铁代谢的靶向疗法可有效治疗动脉粥样硬化和其他心血管疾病。
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 去求助
来源期刊
CiteScore
9.00
自引率
3.40%
发文量
87
审稿时长
6-12 weeks
期刊介绍: The aim of this journal is to systematically provide expert views on current basic science and clinical advances in the field of atherosclerosis and highlight the most important developments likely to transform the field of cardiovascular prevention, diagnosis, and treatment. We accomplish this aim by appointing major authorities to serve as Section Editors who select leading experts from around the world to provide definitive reviews on key topics and papers published in the past year. We also provide supplementary reviews and commentaries from well-known figures in the field. An Editorial Board of internationally diverse members suggests topics of special interest to their country/region and ensures that topics are current and include emerging research.
期刊最新文献
Myopathy in Statin-Treated Children and Adolescents: A Practical Approach. "Improving Diet Quality of Children with Dyslipidemia Who also Exhibit Picky Eating Behaviors". Transitioning Adolescents and Young Adults with Lipid Disorders to Adult Health Care. PCSK9 Monoclonal Antibodies Have Come a Long Way. Pericoronary Fat Attenuation: Diagnosis and Clinical Implications.
×
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