组蛋白去乙酰化酶在调节心肌肥大过程中的作用机制

doi:10.16288/j.yczz.19-346

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Hereditas(Beijing) ›› 2020, Vol. 42 ›› Issue (6): 536-547.doi: 10.16288/j.yczz.19-346

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The mechanism underlying histone deacetylases regulating cardiac hypertrophy

Lian Ren, Xiushan Wu, Yongqing Li()

State Key Lab of Development Biology of Freshwater Fish, Key Laboratory of the Ministry of Education, Heart Development Research Center, College of Life Sciences, Hunan Normal University, Changsha 410081, China

Received:2020-01-18 Revised:2020-04-13 Online:2020-06-20 Published:2020-04-27
Contact: Li Yongqing E-mail:liyongqing2002cn@aliyun.com
Supported by:
Supported by the National Natural Science Foundation of China No(81470377);Hunan Province Biological Development Engineering and New Product R & D Collaborative Innovation Center No(2013-448-6)

Abstract

Abstract:

Cardiac hypertrophy is a compensatory response that occurs as a result of increased hemodynamic requirement in peripheral tissues. In the process of cardiac hypertrophy, the expression of different types of genes in different stages is transcriptionally regulated by multiple-level physiological and pathological signals. Histone acetylation, as the most extensive post-translational modification, is closely controlled by the antagonistic histone acetyltransferases (HAT) and histone deacetylases (HDACs). Recent studies have shown that HDACs, as a family of enzymes that inhibit transcription and contain highly conserved deacetylase domains, regulate gene expression during cardiac hypertrophy through a variety of pathways. In this review, we mainly summarize the research progress on histone deacetylase in cardiac hypertrophy. By elucidating the role and molecular mechanism of different HDACs in cardiac hypertrophy, it provides new ideas for the treatment of different types of cardiac hypertrophy and heart failure, and molecular targets for new drug design.

Key words: myocardial hypertrophy, post-translational modification, transcription process, histone deacetylases, molecular mechanism

Lian Ren, Xiushan Wu, Yongqing Li. The mechanism underlying histone deacetylases regulating cardiac hypertrophy[J]. Hereditas(Beijing), 2020, 42(6): 536-547.

Figures/Tables 4

Table 1

Fig. 1

Fig. 2

Fig. 3

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	曹继红, 廖尉廷, 沃琤, 徐国荣, 徐焕新, 李平龙, 陶冶, 王鹏, 林加日, 邓连瑞 . 组蛋白去乙酰化酶抑制剂影响的代谢相关基因的组学筛查及验证. 遗传, 2015,37(9):918-925.

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HDACs亚族	分子结构	研究模型	参考文献
I类	HDAC1 482 aa	HDAC1敲除小鼠模型	[8~12]
	HDAC2 488 aa	HDAC2敲除/转基因小鼠模型	[8~9,13~20]
	HDAC3 428 aa	HDAC3转基因小鼠模型	[8,21~23]
	HDAC8 377 aa	高血压大鼠模型	[20,24,25]
IIa类	HDAC4 1084 aa	Dvl1转基因CaMKII敲除小鼠模型	[26,27]
	HDAC5 1122 aa	HDAC5敲除/转基因小鼠模型	[26,28~33]
	HDAC7 952 aa	-
	HDAC9 1011 aa	HDAC9敲除小鼠模型	[34,35]
IIb类	HDAC6 1215 aa	HDAC6敲除小鼠模型	[24,33,36,37]
IIb类	HDAC10 669 aa	-
IV类	HDAC11 347 aa	-
III类	SIRT1 747 aa	SIRT1敲除小鼠模型	[38~41]
	SIRT2 389 aa	SIRT2敲除/转基因小鼠模型	[42]
	SIRT3 399 aa	SIRT3敲除/转基因小鼠模型	[43~45]
	SIRT4 314 aa	SIRT4敲除/转基因小鼠模型	[46]
	SIRT5 310 aa	SIRT5敲除小鼠模型	[47,48]
	SIRT6 355 aa	SIRT6转基因小鼠模型	[49]
	SIRT7 400 aa	SIRT7心脏特异敲除小鼠模型	[50]

The mechanism underlying histone deacetylases regulating cardiac hypertrophy

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