心肌肥大表观遗传调控的研究进展

doi:10.16352/j.issn.1001-6325.2022.03.011

基础医学与临床 ›› 2022, Vol. 42 ›› Issue (3): 520-524.doi: 10.16352/j.issn.1001-6325.2022.03.011

心肌肥大表观遗传调控的研究进展

郑婧婧¹, 卜宁¹, 赵钊¹, 张佳靖², 于慧¹, 赵宇航^1*

1.包头医学院, 内蒙古包头 014000;
2.内蒙古包钢疗养院,内蒙古包头 014000

收稿日期:2021-07-15 修回日期:2021-11-15 出版日期:2022-03-05 发布日期:2022-03-04
通讯作者: ^* idealgas@foxmail.com
基金资助:
内蒙古自然科学基金(2017BS0301); 内蒙古教育厅科技项目(NJZY17260); 包头医学院扬帆计划(BYJJ-YF201625); 内蒙古自治区商校“青年科技英才”支持计划(NJYT-20-B34);包头医学院研究生科研创新项目(bycx2020005)

Progress in the study of the epigenetic regulation of cardiac hypertrophy

ZHENG Jing-jing¹, BU Ning¹, ZHAO Zhao¹, ZHANG Jia-jing², YU Hui¹, ZHAO Yu-hang^1*

1. Baotou Medical College,Baotou 014000;
2. Inner Mongolia Baotou Steel Sanatorium,Baotou 014000,China

Received:2021-07-15 Revised:2021-11-15 Online:2022-03-05 Published:2022-03-04
Contact: ^* idealgas@foxmail.com

摘要/Abstract

摘要： 心肌肥大是各种严重心血管疾病的独立危险因素。表观遗传学涉及的机制,如DNA甲基化、组蛋白修饰、RNA甲基化等参与心肌肥大的发生发展。因此,了解表观遗传对心肌肥大的作用有助于为心肌肥大的预防和早期治疗提供有效方案和科学依据。

关键词: 心肌肥大, 表观遗传学, 非编码RNA, DNA甲基化, 组蛋白修饰

Abstract: Myocardial hypertrophy is an independent risk factor for various serious cardiovascular diseases.Epigenetic mechanisms such as DNA methylation, histone modification, and RNA methylation are involved in the pathogenesis and development of cardiac hypertrophy.To understanding the role of epigenetic regulation on cardiac hypertrophy contributes to to development of an effective protocol and provide scientific basis for the prevention and early treatment of cardiac hypertrophy.

Key words: myocardial hypertrophy, epigenetics, noncoding RNA, DNA methylation, histone modification

中图分类号:

郑婧婧, 卜宁, 赵钊, 张佳靖, 于慧, 赵宇航. 心肌肥大表观遗传调控的研究进展[J]. 基础医学与临床, 2022, 42(3): 520-524.

ZHENG Jing-jing, BU Ning, ZHAO Zhao, ZHANG Jia-jing, YU Hui, ZHAO Yu-hang. Progress in the study of the epigenetic regulation of cardiac hypertrophy[J]. Basic & Clinical Medicine, 2022, 42(3): 520-524.

参考文献

[1]Benjamin EJ, Muntner P, Alonso A, et al. Heart disease and stroke statistics-2019 update: a report from the american heart association[J]. Circulation, 2019, 139: e56-e528.
[2]Dong Y, Xu S, Liu J, et al. Non-coding RNA-linked epigenetic regulation in cardiac hypertrophy[J]. Int J Biol Sci, 2018, 149: 1133-1141.
[3]Xiao D, Dasgupta C, Chen M, et al. Inhibition of DNA methylation reverses norepinephrine-induced cardiac hypertrophy in rats[J]. Cardiovasc Res, 2014, 1013: 373-382.
[4]Stenzig J, Schneeberger Y, Loser A, et al. Pharmacologi-cal inhibition of DNA methylation attenuates pressure overload-induced cardiac hypertrophy in rats[J]. J Mol Cell Cardiol, 2018, 120: 53-63.
[5]陈美婷, 张弋, 江慧琳, 等. 5-氮杂胞苷抑制血管紧张素Ⅱ诱导心肌肥大的作用研究[J].中华急诊医学杂志,2018, 273: 301-306.
[6]Liu L, He X, Zhao M, et al. Regulation of DNA methylation and 2-OG/TET signaling by choline alleviated cardiac hypertrophy in spontaneously hypertensive rats[J]. J Mol Cell Cardiol, 2019, 128: 26-37.
[7]Ooi JY, Tuano NK, Rafehi H, et al. Hdac inhibition attenuates cardiac hypertrophy by acetylation and deacetylation of target genes[J]. Epigenetics, 2015, 105: 418-430.
[8]Kee HJ, Sohn IS, Nam KI, et al. Inhibition of histone deacetylation blocks cardiac hypertrophy induced by angiotensin Ⅱ infusion and aortic banding[J]. Circulation, 2006, 1131: 51-59.
[9]Ferguson BS, Harrison BC, Jeong MY, et al. Signal-dependent repression of DUSP5 by class Ⅰ HDACs controls nuclear ERK activity and cardiomyocyte hypertrophy[J]. Proc Natl Acad Sci U S A, 2013, 11024: 9806-9811.
[10]Lee E, Song MJ, Lee HA, et al. Histone deacetylase inhibitor, cg200745, attenuates cardiac hypertrophy and fibrosis in DOCA-induced hypertensive rats[J]. Korean J Physiol Pharmacol, 2016, 205: 477-485.
[11]Lee E, Lee HA, Kim M, et al. Upregulation of C/EBPB and TSC2 by an HDAC inhibitor cg200745 protects heart from DOCA-induced hypertrophy[J]. Clin Exp Pharmacol Physiol, 2019, 463: 226-236.
[12]Dorn LE, Tual-Chalot S, Stellos K, et al. RNA epigenetics and cardiovascular diseases[J]. J Mol Cell Cardiol, 2019, 129: 272-280.
[13]Paramasivam A, Vijayashree Priyadharsini J, Raghunandhakumar S. N6-adenosine methylation (m6A): a promising new molecular target in hypertension and cardiovascular diseases[J]. Hypertens Res, 2020, 432: 153-154.
[14]Ni H, Li W, Zhuge Y, et al. Inhibition of circhipk3 prevents angiotensin Ⅱ-induced cardiac fibrosis by sponging mIR-29b-3p[J]. Int J Cardiol, 2019, 292: 188-196.
[15]Dorn LE, Lasman L, Chen J, et al. The n(6)-methyladenosine mRNA methylase mettl3 controls cardiac homeo-stasis and hypertrophy[J]. Circulation, 2019, 1394: 533-545.
[16]Gao XQ, Zhang YH, Liu F, et al. The PiRNA chapir regulates cardiac hypertrophy by controlling mettl3-dependent n(6)-methyladenosine methylation of parp10 mRNA[J]. Nat Cell Biol, 2020, 2211: 1319-1331.
[17]Sun T, Dong YH, Du W, et al. The role of microRNAs in myocardial infarction: from molecular mechanism to clinical application[J]. Int J Mol Sci, 2017,18:745.doi:10.3390/ijms18040745.
[18]Xu X, Su YL, Shi JY, et al. MicroRNA-17-5p promotes cardiac hypertrophy by targeting mfn2 to inhibit autophagy[J]. Cardiovasc Toxicol, 2021, 219: 759-771.
[19]Ding YQ, Zhang YH, Lu J, et al. MicroRNA-214 contributes to ang II-induced cardiac hypertrophy by targeting sirt3 to provoke mitochondrial malfunction[J]. Acta Pharmacol Sin, 2021, 429: 1422-1436.
[20]Zeng J, Wang L, Zhao J, et al. miR-100-5p regulates cardiac hypertrophy through activation of autophagy by targeting mtor[J]. Hum Cell, 2021, 345: 1388-1397.
[21]Qi J, Luo X, Ma Z, et al. Downregulation of miR-26b-5p, miR-204-5p, and miR-497-3p expression facilitates exercise-induced physiological cardiac hypertrophy by augmenting autophagy in rats[J]. Front Genet, 2020, 11: 78.doi: 10.3389/fgene.2020.00078.
[22]Thum T, Condorelli G. Long noncoding RNAs and mic-roRNAs in cardiovascular pathophysiology[J]. Circ Res, 2015, 1164: 751-762.
[23]Zou X, Wang J, Tang L, et al. LncRNA tug1 contributes to cardiac hypertrophy via regulating miR-29b-3p[J]. In Vitro Cell Dev Biol Anim, 2019, 557: 482-490.
[24]Wo Y, Guo J, Li P, et al. Long non-coding RNA chrf facilitates cardiac hypertrophy through regulating Akt3 via miR-93[J]. Cardiovasc Pathol, 2018, 35: 29-36.
[25]Xu Y, Luo Y, Liang C, et al. LncRNA-mhrt regulates cardiac hypertrophy by modulating the miR-145a-5p/klf4/myocardin axis[J]. J Mol Cell Cardiol, 2020, 139: 47-61.
[26]Song C, Qi H, Liu Y, et al. Inhibition of lncRNA gm15834 attenuates autophagy-mediated myocardial hypertrophy via the miR-30b-3p/ulk1 axis in mice[J]. Mol Ther, 2021, 293: 1120-1137.
[27]Wang K, Long B, Liu F, et al. A circular RNA protects the heart from pathological hypertrophy and heart failure by targeting miR-223[J]. Eur Heart J, 2016, 3733: 2602-2611.
[28]Li H, Xu JD, Fang XH, et al. Circular RNA circRNA_000203 aggravates cardiac hypertrophy via suppressing miR-26b-5p and miR-140-3p binding to gata4[J]. Cardiovasc Res, 2020, 1167: 1323-1334.
[29]Xu X, Wang J, Wang X. Silencing of circHIPK3 inhibits pressure overload-induced cardiac hypertrophy and dysfunction by sponging miR-185-3p[J]. Drug Des Devel Ther, 2020, 14: 5699-5710.
[30]Lim TB, Aliwarga E, Luu TDA, et al. Targeting the highly abundant circular RNA circSLC8A1 in cardio-myocytes attenuates pressure overload induced hypertrophy[J]. Cardiovasc Res, 2019, 11514: 1998-2007.

心肌肥大表观遗传调控的研究进展

Progress in the study of the epigenetic regulation of cardiac hypertrophy

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