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N6-甲基腺苷修饰在心脏重塑中的作用。

Role of N6-methyladenosine Modification in Cardiac Remodeling.

作者信息

Choy ManTing, Xue Ruicong, Wu Yuzhong, Fan Wendong, Dong Yugang, Liu Chen

机构信息

Department of Cardiology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.

National Health Commission (NHC) Key Laboratory of Assisted Circulation, Sun Yat-sen University, Guangzhou, China.

出版信息

Front Cardiovasc Med. 2022 Feb 10;9:774627. doi: 10.3389/fcvm.2022.774627. eCollection 2022.

DOI:10.3389/fcvm.2022.774627
PMID:35224032
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8866307/
Abstract

Cardiac remodeling is the critical process in heart failure due to many cardiovascular diseases including myocardial infarction, hypertension, cardiovascular disease and cardiomyopathy. However, treatments for heart failure focusing on cardiac remodeling show relatively limited effectiveness. In recent decades, epitranscriptomic modifications were found abundantly present throughout the progression of cardiac remodeling, and numerous types of biochemical modifications were identified. m6A modification is the methylation of the adenosine base at the nitrogen-6 position, and dysregulation of m6A modification has been implicated in a wide range of diseases. However, function of m6A modifications still remain largely unknown in cardiac diseases, especially cardiac remodeling. LncRNAs are also shown to play a vital role in the pathophysiology of cardiac remodeling and heart failure. The crosstalk between lncRNAs and m6A modification provides a novel prospective for exploring possible regulatory mechanism and therapeutic targets of cardiac remodeling. This review summarizes the role of m6A modification in cardiac remodeling in the current researches.

摘要

心脏重塑是许多心血管疾病(包括心肌梗死、高血压、心血管疾病和心肌病)导致心力衰竭的关键过程。然而,针对心脏重塑的心力衰竭治疗效果相对有限。近几十年来,人们发现表观转录组修饰在心脏重塑过程中大量存在,并鉴定出多种类型的生化修饰。m6A修饰是腺苷碱基在氮-6位置的甲基化,m6A修饰失调与多种疾病有关。然而,m6A修饰在心脏疾病尤其是心脏重塑中的功能仍 largely未知。长链非编码RNA(lncRNAs)也在心脏重塑和心力衰竭的病理生理学中发挥着重要作用。lncRNAs与m6A修饰之间的相互作用为探索心脏重塑可能的调控机制和治疗靶点提供了新的前景。本综述总结了当前研究中m6A修饰在心脏重塑中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2582/8866307/9626654237ad/fcvm-09-774627-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2582/8866307/9626654237ad/fcvm-09-774627-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2582/8866307/9626654237ad/fcvm-09-774627-g0001.jpg

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STING protects against cardiac dysfunction and remodelling by blocking autophagy.STING 通过阻断自噬来保护心脏功能和重塑。
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FTO overexpression inhibits apoptosis of hypoxia/reoxygenation-treated myocardial cells by regulating m6A modification of Mhrt.FTO 过表达通过调节 Mhrt 的 m6A 修饰抑制缺氧/复氧处理的心肌细胞凋亡。
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Remodeling of the mA landscape in the heart reveals few conserved post-transcriptional events underlying cardiomyocyte hypertrophy.心脏中 mA 景观的重塑揭示了很少有保守的心脏细胞肥大的转录后事件。
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