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蛋白质精氨酸甲基转移酶与心血管疾病的关系(综述)

Relationship between protein arginine methyltransferase and cardiovascular disease (Review).

作者信息

Zheng Sisi, Zeng Congcong, Huang Ailing, Huang Fuqi, Meng Anna, Wu Zhuan, Zhou Shouhong

机构信息

Guangxi Key Laboratory of Brain and Cognitive Neuroscience, Guilin Medical University, Guilin, Guangxi 541199, P.R. China.

Central Laboratory, Guangxi Health Commission Key Laboratory of Glucose and Lipid Metabolism Disorders, The Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541199, P.R. China.

出版信息

Biomed Rep. 2022 Sep 16;17(5):90. doi: 10.3892/br.2022.1572. eCollection 2022 Nov.

DOI:10.3892/br.2022.1572
PMID:36237286
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9500492/
Abstract

Protein arginine methyltransferases (PRMTs) are widely found in eukaryotes and regulate gene expression and post-translational modifications. PRMT1-PRMT6 have important roles in the pathology of cardiovascular diseases (CVDs), including atherosclerosis, heart failure and myocardial hypertrophy. Although these enzymes are also closely associated with various CVDs, the mechanisms of the involvement of PRMTs in the regulation of CVD have remained largely elusive. PRMTs methylate arginine residues and other factors. The present review describes the roles of PRMT1-PRMT6 in CVD. Furthermore, the biological characteristics of PRMTs and mechanisms by which PRMTs regulate cholesterol metabolism are being introduced. This review aims to provide inspiration for cardiovascular drug research and offer clues for research on the pathogenesis of CVD.

摘要

蛋白质精氨酸甲基转移酶(PRMTs)广泛存在于真核生物中,可调节基因表达和翻译后修饰。PRMT1 - PRMT6在心血管疾病(CVDs)的病理过程中发挥重要作用,包括动脉粥样硬化、心力衰竭和心肌肥大。尽管这些酶也与多种心血管疾病密切相关,但PRMTs参与心血管疾病调节的机制在很大程度上仍不清楚。PRMTs使精氨酸残基和其他因子发生甲基化。本综述描述了PRMT1 - PRMT6在心血管疾病中的作用。此外,还介绍了PRMTs的生物学特性以及PRMTs调节胆固醇代谢的机制。本综述旨在为心血管药物研究提供启发,并为心血管疾病发病机制的研究提供线索。

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J Cell Physiol. 2022 Jul;237(7):3069-3079. doi: 10.1002/jcp.30775. Epub 2022 May 17.
2
PRMT7 ablation in cardiomyocytes causes cardiac hypertrophy and fibrosis through β-catenin dysregulation.心肌细胞中 PRMT7 的缺失会导致β-连环蛋白失调,引起心肌肥厚和纤维化。
Cell Mol Life Sci. 2022 Jan 28;79(2):99. doi: 10.1007/s00018-021-04097-x.
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PRMT5 confers lipid metabolism reprogramming, tumour growth and metastasis depending on the SIRT7-mediated desuccinylation of PRMT5 K387 in tumours.PRMT5 通过 SIRT7 介导的 PRMT5 K387 脱琥珀酰化作用来调节肿瘤中的脂质代谢重编程、肿瘤生长和转移。
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4
Depletion of m A reader protein YTHDC1 induces dilated cardiomyopathy by abnormal splicing of Titin.m A 读者蛋白 YTHDC1 的耗竭通过肌联蛋白的异常剪接诱导扩张型心肌病。
J Cell Mol Med. 2021 Dec;25(23):10879-10891. doi: 10.1111/jcmm.16955. Epub 2021 Oct 30.
5
Histone Methylation Related Therapeutic Challenge in Cardiovascular Diseases.心血管疾病中组蛋白甲基化相关的治疗挑战
Front Cardiovasc Med. 2021 Sep 9;8:710053. doi: 10.3389/fcvm.2021.710053. eCollection 2021.
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