索引超出了数组界限。 文章摘要
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[1]彭昌,田杰.组蛋白乙酰化修饰失衡在心肌肥厚中的作用[J].国际心血管病杂志,2016,05:283-285.
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组蛋白乙酰化修饰失衡在心肌肥厚中的作用(PDF)

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

期数:
2016年05期
页码:
283-285
栏目:
综述
出版日期:
2016-09-20

文章信息/Info

Title:
-
作者:
彭昌; 田杰
563000 遵义医学院附属医院儿科(彭 昌); 400014 重庆医科大学附属儿童医院心内科(田 杰)
Author(s):
-
关键词:
表观遗传学; 组蛋白乙酰化; 心肌肥厚
Keywords:
-
分类号:
-
DOI:
10.3969/j.issn.1673-6583.2016.05.008
文献标识码:
-
摘要:
心肌肥厚是多种心血管疾病发生发展过程中的一个重要阶段。组蛋白乙酰化修饰失衡参与了心肌肥厚的发病过程,多种组蛋白乙酰化酶可调控心脏发育相关转录因子的转录活性,而组蛋白乙酰化酶特异性抑制剂能够逆转组蛋白高乙酰化状态并修复这一病理过程。该文主要介绍表观遗传学中组蛋白乙酰化酶介导的组蛋白乙酰化修饰失衡对心肌肥厚的影响。
Abstract:
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参考文献/References

[1] Greco CM, Condorelli G. Epigenetic modifications and noncoding RNAs in cardiac hypertrophy and failure [J]. Nat Rev Cardiol, 2015,12(8):488-497.
[2] Wang Y, Miao X, Liu Y, et al. Dysregulation of histone acetyltransferases and deacetylases in cardiovascular diseases [J]. Oxid Med Cell Longev, 2014,2014:641979.
[3] 曹珊珊, 苏永立, 李瑞芳, 等. Ⅰ型组蛋白去乙酰化酶在心肌肥厚中的靶点作用[J]. 国际心血管病杂志, 2013,40(6):359-361.
[4] Sadoul K, Boyault C, Pabion M, et al. Regulation of protein turnover by acetyltransferases and deacetylases [J]. Biochimie, 2008,90(2):306-312.
[5] Yang XJ, Seto E. HATs and HDACs: from structure, function and regulation to novel strategies for therapy and prevention [J]. Oncogene, 2007,26(37):5310-5318.
[6] Mujtaba S, Zeng L, Zhou MM. Structure and acetyl-lysine recognition of the bromodomain [J]. Oncogene, 2007,26(37):5521-5527.
[7] Wei JQ, Shehadeh LA, Mitrani JM, et al. Quantitative control of adaptive cardiac hypertrophy by acetyltransferase p300 [J]. Circulation, 2008,118(9):934-946.
[8] Chen X, Qin L, Liu Z, et al. Knockout of SRC-1 and SRC-3 in mice decreases cardiomyocyte proliferation and causes a noncompaction cardiomyopathy phenotype [J]. Int J Biol Sci, 2015,11(9):1056-1072.
[9] Li L, Zhu J, Tian J, et al. A role for Gcn5 in cardiomyocyte differentiation of rat mesenchymal stem cells [J]. Mol Cell Biochem, 2010,345(1-2):309-316.
[10] Lin W, Srajer G, Evrard YA, et al. Developmental potential of Gcn5(-/-)embryonic stem cells in vivo and in vitro [J]. Dev Dyn, 2007,236(6):1547-1557.
[11] Cao Y, Lu L, Liu M, et al. Impact of epigenetics in the management of cardiovascular disease: a review [J]. Eur Rev Med Pharmacol Sci, 2014,18(20):3097-3104.
[12] Li HL, Liu C, de Couto G, et al. Curcumin prevents and reverses murine cardiac hypertrophy [J]. J Clin Invest, 2008,118(3):879-893.
[13] Weber D, Heisig J, Kneitz S, et al. Mechanisms of epigenetic and cell-type specific regulation of Hey target genes in ES cells and cardiomyocytes [J]. J Mol Cell Cardiol, 2015,79:79-88.
[14] Peng C, Zhu J, Sun HC, et al. Inhibition of histone H3K9 acetylation by anacardic acid can correct the over-expression of Gata4 in the hearts of fetal mice exposed to alcohol during pregnancy [J]. PLoS One, 2014,9(8):e104135.
[15] Gao W, Pan B, Liu L, et al. Alcohol exposure increases the expression of cardiac transcription factors through ERK1/2-mediated histone3 hyperacetylation in H9c2 cells [J]. Biochem Biophys Res Commun, 2015,466(4):670-675.
[16] Backs J, Olson EN. Control of cardiac growth by histone acetylation/deacetylation [J]. Circ Res, 2006,98(1):15-24.
[17] Shen P, Feng X, Zhang X, et al. SIRT6 suppresses phenylephrine-induced cardiomyocyte hypertrophy though inhibiting p300 [J]. J Pharmacol Sci, 2016 Apr 1. [Epub ahead of print].
[18] Suzuki H, Katanasaka Y, Sunagawa Y, et al. Tyrosine phosphorylation of RACK1 triggers cardiomyocyte hypertrophy by regulating the interaction between p300 and GATA4 [J]. Biochim Biophys Acta, 2016,1862(9):1544-1557.
[19] Peng C, Zhang W, Zhao W, et al. Alcohol-induced histone H3K9 hyperacetylation and cardiac hypertrophy are reversed by a histone acetylases inhibitor anacardic acid in developing murine hearts [J]. Biochimie, 2015,113(3):1-9.
[20] Chowdhury R, Nimmanapalli R, Graham T, et al. Curcumin attenuation of lipopolysaccharide induced cardiac hypertrophy in rodents [J]. ISRN Inflamm, 2013,2013:539305.
[21] 周瑶瑶, 张俊峰. 姜黄素在心血管疾病中的应用[J]. 国际心血管病杂志, 2015,42(1):41-43.
[22] Eom GH, Nam YS, Oh JG, et al. Regulation of acetylation of histone deacetylase 2 by p300/CBP-associated factor/histone deacetylase 5 in the development of cardiac hypertrophy [J]. Circ Res, 2014,114(7):1133-1143.
[23] Papait R, Cattaneo P, Kunderfranco P, et al. Genome-wide analysis of histone marks identifying an epigenetic signature of promoters and enhancers underlying cardiac hypertrophy [J]. Proc Natl Acad Sci U S A, 2013,110(50):20164-20169.
[24] 彭 昌, 张维华, 潘 博, 等. 组蛋白乙酰化酶对心脏发育核心转录因子Mef2c的动态调控作用[J]. 中国当代儿科杂志, 2014,16(4):418-423.
[25] Gusterson RJ, Jazrawi E, Adcock IM, et al. The transcriptional co-activators CREB-binding protein(CBP)and p300 play a critical role in cardiac hypertrophy that is dependent on their histone acetyltransferase activity [J]. J Biol Chem, 2003,278(9):6838-6847.
[26] Lin YH, Warren CM, Li J, et al. Myofibril growth during cardiac hypertrophy is regulated through dual phosphorylation and acetylation of the actin capping protein CapZ [J]. Cell Signal, 2016,28(8):1015-1024.
[27] Qiao W, Zhang W, Gai Y, et al. The histone acetyltransferase MOF overexpression blunts cardiac hypertrophy by targeting ROS in mice [J]. Biochem Biophys Res Commun, 2014,448(4):379-384.
[28] Voelter-Mahlknecht S. Epigenetic associations in relation to cardiovascular prevention and therapeutics [J]. Clin Epigenetics, 2016,8:4.

备注/Memo

备注/Memo:
基金项目:国家自然科学基金(81560040) 作者单位:563000 遵义医学院附属医院儿科(彭 昌); 400014 重庆医科大学附属儿童医院心内科(田 杰) 通信作者:彭 昌,Email: pengchang_2006@126.com
更新日期/Last Update: 2016-09-20