索引超出了数组界限。 文章摘要
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[1]汤宇 喻溥蛟 许嘉鸿.N6-甲基嘌呤介导的RNA甲基化修饰与心血管疾病[J].国际心血管病杂志,2020,05:290-292.
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N6-甲基嘌呤介导的RNA甲基化修饰与心血管疾病(PDF)

《国际心血管病杂志》[ISSN:1006-6977/CN:61-1281/TN]

期数:
2020年05期
页码:
290-292
栏目:
综述
出版日期:
2020-10-15

文章信息/Info

Title:
-
作者:
汤宇 喻溥蛟 许嘉鸿
上海 200065,同济大学附属同济医院心内科
Author(s):
-
关键词:
RNA;  甲基化;  N6-甲基嘌呤;  心血管疾病
Keywords:
-
分类号:
-
DOI:
10.3969/j.issn.1673-6583.2020.05.009
文献标识码:
-
摘要:
N6-甲基嘌呤(m6A)甲基化修饰是RNA最主要的转录后修饰方式,是一种由甲基化转移酶、去甲基化酶以及识别蛋白共同催化的动态可逆的修饰方式,对RNA的转录有重要的调控作用。该文介绍了m6A介导的RNA甲基化修饰在高血压、心脏再灌注损伤及心室重构中的研究进展。
Abstract:
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参考文献/References

[1] Boccaletto P, Machnicka MA, Purta E, et al. MODOMICS: a database of RNA modification pathways. 2017 update[J]. Nucleic Acids Res, 2018, 46(D1):D303-D307.
[2] Blanco S, Frye M. Role of RNA methyltransferases in tissue renewal and pathology[J]. Curr Opin Cell Biol, 2014, 31:1-7.
[3] Desrosiers R, Friderici K, Rottman F. Identification of methylated nucleosides in messenger RNA from novikoff hepatoma cells[J]. Proc Natl Acad Sci U S A, 1974, 71(10):3971-3975.
[4] Dominissini D, Moshitch-Moshkovitz S, Schwartz S, et al. Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq [J]. Nature, 2012, 485(7397):201-206.
[5] Meyer KD, Saletore Y, Zumbo P, et al. Comprehensive analysis of mRNA methylation reveals enrichment in 3' UTRs and near stop codons [J].Cell, 2012, 149(7):1635-1646.
[6] Batista PJ. The RNA modification N(6)-methyladenosine and its implications in human disease[J]. Genom Proteom Bioinf, 2017, 15(3):154-163.
[7] Li Y, Wang J, Huang C, et al. RNA N6-methyladenosine: a promising molecular target in metabolic diseases[J]. Cell Biosci, 2020, 10:19.
[8] Kmietczyk V, Riechert E, Kalinski L, et al. M(6)A-mRNA methylation regulates cardiac gene expression and cellular growth[J]. Life Sci Alliance, 2019, 2(2):e201800233.
[9] Jiang S, Xie Y, He Z, et al. m6ASNP: a tool for annotating genetic variants by m6A function[J]. Gigascience, 2018, 7(5):giy035.
[10] Mo XB, Lei SF, Zhang YH, et al. Examination of the associations between m6A-associated single-nucleotide polymorphisms and blood pressure[J]. Hypertens Res, 2019, 42(10):1582-1589..
[11] Kong H, Li X, Zhang S, et al. The β1-adrenoreceptor gene Arg389Gly and Ser49Gly polymorphisms and hypertension: a meta-analysis[J]. Mol Biol Rep, 2013, 40(6):4047-4053.
[12] Wang H, Liu J, Liu K, et al. β1-adrenoceptor gene Arg389Gly polymorphism and essential hypertension risk in general population: a meta-analysis[J]. Mol Biol Rep, 2013, 40(6):4055-4063.
[13] Sun Y, Sun J, Wu J, et al. Combined effects of FTO rs9939609 and MC4R rs17782313 on elevated nocturnal blood pressure in the Chinese Han population[J]. Cardiovasc J Afr, 2016, 27(1):21-24.
[14] Su H, Wang G, Wu L, et al. Transcriptome-wide map of m(6)A circRNAs identified in a rat model of hypoxia mediated pulmonary hypertension[J]. BMC Genomics, 2020, 21(1):39.
[15] Braunwald E, Kloner RA. Myocardial reperfusion: a double-edged sword?[J]. J Clin Invest, 1985, 76(5):1713-1719.
[16] Bugiardini R. Coronary microcirculation and ischemic heart disease, today[J]. Curr Pharm Des, 2018, 24(25):2891-2892.
[17] Fry NJ, Law BA, Ilkayeva OR, et al. N(6)-methyladenosine is required for the hypoxic stabilization of specific mRNAs[J]. RNA, 2017, 23(9):1444-1455.
[18] Wang J, Ishfaq M, Xu L, et al. METTL3/m(6)A/miRNA-873-5p attenuated oxidative stress and apoptosis in colistin-induced kidney injury by modulating Keap1/Nrf2 pathway[J]. Front Pharmacol, 2019, 10:517.
[19] Song H, Feng X, Zhang H, et al. METTL3 and ALKBH5 oppositely regulate m(6)A modification of TFEB mRNA, which dictates the fate of hypoxia/reoxygenation-treated cardiomyocytes[J]. Autophagy, 2019, 15(8):1419-1437.
[20] Wu L, Pei Y, Zhu Y, et al. Association of N(6)-methyladenine DNA with plaque progression in atherosclerosis via myocardial infarction-associated transcripts[J]. Cell Death Dis, 2019, 10(12):909.
[21] Dorn LE, Lasman L, Chen J, et al. The N(6)-methyladenosine mRNA methylase METTL3 controls cardiac homeostasis and hypertrophy[J]. Circulation, 2019, 139(4):533-545.
[22] Mathiyalagan P, Adamiak M, Mayourian J, et al. FTO-dependent N(6)-methyladenosine regulates cardiac function during remodeling and repair[J]. Circulation, 2019, 139(4):518-532.
[23] Carnevali L, Graiani G, Rossi S, et al. Signs of cardiac autonomic imbalance and proarrhythmic remodeling in FTO deficient mice[J]. PLoS One, 2014, 9(4):e95499.
[24] Gan XT, Zhao G, Huang CX, et al. Identification of fat mass and obesity associated(FTO)protein expression in cardiomyocytes: regulation by leptin and its contribution to leptin-induced hypertrophy[J]. PLoS One, 2013, 8(9):e74235.
[25] Yang Y, Fan X, Mao M, et al. Extensive translation of circular RNAs driven by N(6)-methyladenosine[J]. Cell Res, 2017, 27(5):626-641.
[26] Gomes CPC, Schroen B, Kuster GM, et al. Regulatory RNAs in heart failure[J]. Circulation, 2020, 141(4):313-328.

备注/Memo

备注/Memo:
通信作者:许嘉鸿,E-mail:xujiahong@tongji.edu.cn
更新日期/Last Update: 2020-10-15