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铁死亡:心血管疾病的一种新策略。

Ferroptosis: a new strategy for cardiovascular disease.

作者信息

Wang Yuyuan, Wu Junduo

机构信息

Department of Cardiology, Second Hospital of Jilin University, Changchun, China.

出版信息

Front Cardiovasc Med. 2023 Sep 4;10:1241282. doi: 10.3389/fcvm.2023.1241282. eCollection 2023.

DOI:10.3389/fcvm.2023.1241282
PMID:37731525
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10507265/
Abstract

Cardiovascular disease (CVD) is currently one of the prevalent causes of human death. Iron is one of the essential trace elements in the human body and a vital component of living tissues. All organ systems require iron for various metabolic processes, including myocardial and skeletal muscle metabolism, erythropoiesis, mitochondrial function, and oxygen transport. Its deficiency or excess in the human body remains one of the nutritional problems worldwide. The total amount of iron in a normal human body is about 3-5 g. Iron deficiency may cause symptoms such as general fatigue, pica, and nerve deafness, while excessive iron plays a crucial role in the pathophysiological processes of the heart through ferroptosis triggered by the Fenton reaction. It differs from other cell death modes based on its dependence on the accumulation of lipid peroxides and REDOX imbalance, opening a new pathway underlying the pathogenesis and mechanism of CVDs. In this review, we describe the latest research progress on the mechanism of ferroptosis and report its crucial role and association with miRNA in various CVDs. Finally, we summarise the potential therapeutic value of ferroptosis-related drugs or ferroptosis inhibitors in CVDs.

摘要

心血管疾病(CVD)是目前人类死亡的主要原因之一。铁是人体必需的微量元素之一,也是活组织的重要组成部分。所有器官系统都需要铁来进行各种代谢过程,包括心肌和骨骼肌代谢、红细胞生成、线粒体功能和氧气运输。人体中铁的缺乏或过量仍然是全球范围内的营养问题之一。正常人体中铁的总量约为3-5克。缺铁可能会导致全身疲劳、异食癖和神经性耳聋等症状,而过量的铁则通过芬顿反应引发的铁死亡在心脏的病理生理过程中起关键作用。它与其他细胞死亡模式不同,因为它依赖于脂质过氧化物的积累和氧化还原失衡,这为心血管疾病的发病机制和机理开辟了一条新途径。在这篇综述中,我们描述了铁死亡机制的最新研究进展,并报告了其在各种心血管疾病中与微小RNA的关键作用及关联。最后,我们总结了铁死亡相关药物或铁死亡抑制剂在心血管疾病中的潜在治疗价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c544/10507265/a9a642e94730/fcvm-10-1241282-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c544/10507265/3e1c68bd5204/fcvm-10-1241282-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c544/10507265/a9a642e94730/fcvm-10-1241282-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c544/10507265/3e1c68bd5204/fcvm-10-1241282-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c544/10507265/a9a642e94730/fcvm-10-1241282-g002.jpg

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本文引用的文献

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Cardiac-specific overexpression of catalase attenuates lipopolysaccharide-induced cardiac anomalies through reconciliation of autophagy and ferroptosis.心脏特异性过表达过氧化氢酶通过协调自噬和铁死亡减轻脂多糖诱导的心脏异常。
Life Sci. 2023 Sep 1;328:121821. doi: 10.1016/j.lfs.2023.121821. Epub 2023 May 29.
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Mesenchymal stem cell-derived extracellular vesicles protect against abdominal aortic aneurysm formation by inhibiting NET-induced ferroptosis.间质干细胞衍生的细胞外囊泡通过抑制 NET 诱导的铁死亡来防止腹主动脉瘤形成。
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铁死亡相关基因在肾透明细胞癌中的生物学功能及预后意义
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Ferroptosis genes and ST-segment elevation myocardial infarction outcomes: A predictive signature.铁死亡基因与ST段抬高型心肌梗死预后:一种预测特征。
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PCSK9, a novel immune and ferroptosis related gene in abdominal aortic aneurysm neck.
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Sci Rep. 2023 Apr 13;13(1):6054. doi: 10.1038/s41598-023-33287-9.
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