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铁死亡作为心血管疾病的一个新的治疗靶点。

Ferroptosis as a novel therapeutic target for cardiovascular disease.

机构信息

Department of Cardiology, The Second Affiliated Hospital of Soochow University, Suzhou, China.

出版信息

Theranostics. 2021 Jan 1;11(7):3052-3059. doi: 10.7150/thno.54113. eCollection 2021.

DOI:10.7150/thno.54113
PMID:33537073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7847684/
Abstract

Cell death is an important component of the pathophysiology of cardiovascular disease. An understanding of how cardiomyocytes die, and why regeneration of cells in the heart is limited, is a critical area of study. Ferroptosis is a form of regulated cell death that is characterized by iron overload, leading to accumulation of lethal levels of lipid hydroperoxides. The metabolism of iron, lipids, amino acids and glutathione tightly controls the initiation and execution of ferroptosis. Emerging evidence shows that ferroptosis is closely associated with the occurrence and progression of various diseases. In recent years, ferroptosis has been found to play critical roles in cardiomyopathy, myocardial infarction, ischemia/reperfusion injury, and heart failure. This article reviews the mechanisms by which ferroptosis is initiated and controlled and discusses ferroptosis as a novel therapeutic target for various cardiovascular diseases.

摘要

细胞死亡是心血管疾病病理生理学的一个重要组成部分。了解心肌细胞如何死亡,以及为什么心脏细胞的再生受到限制,是一个关键的研究领域。铁死亡是一种受调控的细胞死亡形式,其特征是铁过载,导致致命水平的脂质过氧化物积累。铁、脂质、氨基酸和谷胱甘肽的代谢严格控制着铁死亡的起始和执行。新出现的证据表明,铁死亡与各种疾病的发生和进展密切相关。近年来,铁死亡被发现在心衰、心肌梗死、缺血/再灌注损伤和心肌病等疾病中发挥关键作用。本文综述了铁死亡的发生和调控机制,并讨论了铁死亡作为各种心血管疾病的新治疗靶点的可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4ad/7847684/8f369f3d4f1f/thnov11p3052g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4ad/7847684/3f2bc63f00a6/thnov11p3052g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4ad/7847684/8f369f3d4f1f/thnov11p3052g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4ad/7847684/3f2bc63f00a6/thnov11p3052g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4ad/7847684/8f369f3d4f1f/thnov11p3052g002.jpg

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Free Radic Biol Med. 2020 Nov 20;160:303-318. doi: 10.1016/j.freeradbiomed.2020.08.009. Epub 2020 Aug 23.
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USP8 protects rat-derived H9C2 cardiomyocytes from doxorubicin-triggered ferroptosis and cell death through deubiquitination-mediated stabilization of MDM4.USP8通过去泛素化介导的MDM4稳定化作用,保护大鼠来源的H9C2心肌细胞免受阿霉素引发的铁死亡和细胞死亡。
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Advanced Nanomaterial Platforms for Targeted Therapy of Myocardial Ischemia-Reperfusion Injury.用于心肌缺血再灌注损伤靶向治疗的先进纳米材料平台
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