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铁死亡在心房颤动中的作用:前景广阔。

The Role of Ferroptosis in Atrial Fibrillation: A Promising Future.

作者信息

Zhou Jia-Bin, Qian Ling-Ling, Wu Dan, Wang Ru-Xing

机构信息

Department of Cardiology, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, 214023 Wuxi, Jiangsu, China.

出版信息

Rev Cardiovasc Med. 2024 Apr 1;25(4):127. doi: 10.31083/j.rcm2504127. eCollection 2024 Apr.

DOI:10.31083/j.rcm2504127
PMID:39076535
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11264045/
Abstract

Atrial fibrillation (AF) is one of the most common cardiac arrhythmias, with its diagnosis being closely tied to higher rates of cardiovascular morbidity and mortality. AF is associated with a range of dangerous complications including stroke and heart failure, making it a key driver of healthcare spending and a major threat to global public health. The precise mechanisms that govern AF incidence and the onset of related complications, however, remain uncertain. Ferroptotic cell death has been the focus of rising interest in the cardiac arrhythmias, and there is recent evidence supporting a role for atrial ferroptosis as a mediator of AF development. Interventional strategies focused on ferroptotic activity, such as novel ferroptosis inhibitors, have also shown promise as a means of protecting against AF through their ability to reduce iron overload. In this review, we provide a summary of the proposed mechanisms whereby ferroptosis contributes to the pathophysiology of AF and their therapeutic implications.

摘要

心房颤动(AF)是最常见的心律失常之一,其诊断与心血管疾病发病率和死亡率的升高密切相关。AF与一系列危险并发症相关,包括中风和心力衰竭,使其成为医疗保健支出的关键驱动因素以及对全球公共卫生的重大威胁。然而,控制AF发病率和相关并发症发生的精确机制仍不确定。铁死亡细胞死亡一直是心律失常领域日益受到关注的焦点,最近有证据支持心房铁死亡作为AF发展的介导因素发挥作用。专注于铁死亡活性的干预策略,如新型铁死亡抑制剂,也已显示出有望通过减少铁过载来预防AF。在本综述中,我们总结了铁死亡导致AF病理生理学的潜在机制及其治疗意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6836/11264045/01c7bd16ad21/2153-8174-25-4-127-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6836/11264045/01c7bd16ad21/2153-8174-25-4-127-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6836/11264045/01c7bd16ad21/2153-8174-25-4-127-g1.jpg

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本文引用的文献

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Front Physiol. 2023 Aug 31;14:1206527. doi: 10.3389/fphys.2023.1206527. eCollection 2023.
2
Phosphatidylethanolamine aggravates Angiotensin II-induced atrial fibrosis by triggering ferroptosis in mice.磷脂酰乙醇胺通过引发小鼠铁死亡加重血管紧张素 II 诱导的心房纤维化。
Front Pharmacol. 2023 May 23;14:1148410. doi: 10.3389/fphar.2023.1148410. eCollection 2023.
3
The emerging role of ferroptosis in myocardial fibrosis of atrial fibrillation.
铁死亡在心房颤动心肌纤维化中的新作用。
Arch Med Sci. 2023 Feb 24;19(2):507-512. doi: 10.5114/aoms/160941. eCollection 2023.
4
Inhibition of ferroptosis by icariin treatment attenuates excessive ethanol consumption-induced atrial remodeling and susceptibility to atrial fibrillation, role of SIRT1.淫羊藿素通过抑制铁死亡减轻过量乙醇摄入诱导的心房重构和心房颤动易感性,SIRT1 的作用。
Apoptosis. 2023 Apr;28(3-4):607-626. doi: 10.1007/s10495-023-01814-8. Epub 2023 Jan 28.
5
ER stress-associated transcription factor CREB3 is essential for normal Ca, ATP, and ROS homeostasis.内质网应激相关转录因子CREB3对正常的钙、三磷酸腺苷和活性氧稳态至关重要。
Mitochondrion. 2023 Mar;69:10-17. doi: 10.1016/j.mito.2023.01.001. Epub 2023 Jan 7.
6
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