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E2F家族:心肌病领域的一线曙光。

The E2F family: a ray of dawn in cardiomyopathy.

作者信息

Wei Jinwen, Gao Can, Lu Changxu, Wang Lijie, Dong Dan, Sun Mingli

机构信息

College of Exercise and Health, Shenyang Sport University, No.36 Jinqiansong East Road, Shenyang, 110102, Liaoning, People's Republic of China.

Department of Cardiology, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110033, Liaoning, People's Republic of China.

出版信息

Mol Cell Biochem. 2025 Feb;480(2):825-839. doi: 10.1007/s11010-024-05063-4. Epub 2024 Jul 10.

DOI:10.1007/s11010-024-05063-4
PMID:38985251
Abstract

Cardiomyopathies are a group of heterogeneous diseases, characterized by abnormal structure and function of the myocardium. For many years, it has been a hot topic because of its high morbidity and mortality as well as its complicated pathogenesis. The E2Fs, a group of transcription factors found extensively in eukaryotes, play a crucial role in governing cell proliferation, differentiation, and apoptosis, meanwhile their deregulated activity can also cause a variety of diseases. Based on accumulating evidence, E2Fs play important roles in cardiomyopathies. In this review, we describe the structural and functional characteristics of the E2F family and its role in cardiomyocyte processes, with a focus on how E2Fs are associated with the onset and development of cardiomyopathies. Moreover, we discuss the great potential of E2Fs as biomarkers and therapeutic targets, aiming to provide a reference for future research.

摘要

心肌病是一组异质性疾病,其特征是心肌结构和功能异常。多年来,由于其高发病率和死亡率以及复杂的发病机制,它一直是一个热门话题。E2F 是一组在真核生物中广泛发现的转录因子,在调控细胞增殖、分化和凋亡中起关键作用,同时其活性失调也会导致多种疾病。基于越来越多的证据,E2F 在心肌病中发挥重要作用。在本综述中,我们描述了 E2F 家族的结构和功能特征及其在心肌细胞过程中的作用,重点关注 E2F 如何与心肌病的发生和发展相关联。此外,我们讨论了 E2F 作为生物标志物和治疗靶点的巨大潜力,旨在为未来的研究提供参考。

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本文引用的文献

1
Unique Aspects of Hypertrophic Cardiomyopathy in Children.儿童肥厚型心肌病的独特方面。
Can J Cardiol. 2024 May;40(5):907-920. doi: 10.1016/j.cjca.2024.01.013. Epub 2024 Jan 18.
2
Dilated cardiomyopathy: causes, mechanisms, and current and future treatment approaches.扩张型心肌病:病因、发病机制及当前和未来的治疗方法。
Lancet. 2023 Sep 16;402(10406):998-1011. doi: 10.1016/S0140-6736(23)01241-2.
3
Hydrogen sulfide promoted retinoic acid-related orphan receptor α transcription to alleviate diabetic cardiomyopathy.硫化氢促进维甲酸相关孤儿受体α转录以减轻糖尿病心肌病。
Biochem Pharmacol. 2023 Sep;215:115748. doi: 10.1016/j.bcp.2023.115748. Epub 2023 Aug 15.
4
PRMT5 up-regulation improves myocardial hypertrophy by mediating E2F-1/NF-κB/NLRP3 pathway.PRMT5 的上调通过介导 E2F-1/NF-κB/NLRP3 通路改善心肌肥大。
Prev Med. 2023 Jul;172:107553. doi: 10.1016/j.ypmed.2023.107553. Epub 2023 May 20.
5
Pulsed Electromagnetic Fields Combined With Adipose-Derived Stem Cells Protect Ischemic Myocardium by Regulating miR-20a-5p/E2F1/p73 Signaling.脉冲电磁场联合脂肪源性干细胞通过调节 miR-20a-5p/E2F1/p73 信号保护缺血性心肌。
Stem Cells. 2023 Jul 14;41(7):724-737. doi: 10.1093/stmcls/sxad037.
6
Targeting ferroptosis as a promising therapeutic strategy to treat cardiomyopathy.将铁死亡作为一种有前景的治疗策略来治疗心肌病。
Front Pharmacol. 2023 Apr 13;14:1146651. doi: 10.3389/fphar.2023.1146651. eCollection 2023.
7
Role of E2F transcription factor in oral cancer: Recent insight and advancements.E2F 转录因子在口腔癌中的作用:最新的见解和进展。
Semin Cancer Biol. 2023 Jul;92:28-41. doi: 10.1016/j.semcancer.2023.03.004. Epub 2023 Mar 15.
8
Regulated cell death pathways in cardiomyopathy.调控性细胞死亡通路在心肌病中的作用。
Acta Pharmacol Sin. 2023 Aug;44(8):1521-1535. doi: 10.1038/s41401-023-01068-9. Epub 2023 Mar 13.
9
Deregulated E2F Activity as a Cancer-Cell Specific Therapeutic Tool.去调控 E2F 活性作为一种肿瘤细胞特异性治疗工具。
Genes (Basel). 2023 Feb 2;14(2):393. doi: 10.3390/genes14020393.
10
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J Am Coll Cardiol. 2023 Feb 28;81(8):e57-e58. doi: 10.1016/j.jacc.2022.11.058.