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

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

组蛋白去乙酰化酶在调节心肌肥大过程中的作用机制

任恋, 吴秀山, 李永青()

湖南师范大学省部共建淡水鱼类发育生物学国家重点实验室,教育部重点实验室,生命科学学院心脏发育研究中心,长沙 410081

收稿日期:2020-01-18 修回日期:2020-04-13 出版日期:2020-06-20 发布日期:2020-04-27
通讯作者: 李永青 E-mail:liyongqing2002cn@aliyun.com
作者简介:任恋,在读博士研究生,专业方向：分子遗传。E-mail: 82287168@qq.com
基金资助:
国家自然科学基金项目编号(81470377);湖南省生物发育工程及新产品研发协同创新中心项目资助编号(2013-448-6)

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)

摘要/Abstract

摘要：

心肌肥大(cardiac hypertrophy)是由外周组织对血流动力学需求增加而发生的一种代偿性反应。在心肌肥大过程中,不同时期的不同类型的基因表达受到生理和病理信号的多级转录调控。组蛋白乙酰化作为最广泛的翻译后修饰方式,受相互拮抗的组蛋白乙酰化酶(histone acetyltransferases, HAT)和组蛋白去乙酰化酶(histone deacetylases,HDACs)的精细控制。近年来研究表明,HDACs作为一类抑制转录过程并含有高度保守的脱乙酰酶结构域家族酶,通过多种作用途径调控心肌肥大过程中的基因表达。本文主要综述了组蛋白去乙酰化酶调节心肌肥大过程的相关研究进展,通过阐明不同种类HDACs在心肌肥大中的作用和分子机制,为不同类型心肌肥大和心衰的发病治疗提供新的思路,为新药设计提供分子靶点。

关键词: 心肌肥大, 转录调控, 翻译后修饰, 组蛋白去乙酰化酶, 分子机制

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

任恋, 吴秀山, 李永青. 组蛋白去乙酰化酶在调节心肌肥大过程中的作用机制[J]. 遗传, 2020, 42(6): 536-547.

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

图/表 4

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参考文献 83

[1]	Hunter DJ, Reddy KS . Noncommunicable diseases. N Engl J Med, 2013,369(14):1336-1343.
[2]	Kouzarides T . Acetylation: a regulatory modification to rival phosphorylation? EMBO J, 2000,19(6):1176-1179.
[3]	Taunton J, Hassig CA, Schreiber SL . A mammalian histone deacetylase related to the yeast transcriptional regulator Rpd3p. Science, 1996,272(5260):408-411.
[4]	Jones P, Altamura S, De Francesco R, Gallinari P, Lahm A, Neddermann P, Rowley M, Serafini S, Steinkühler C . Probing the elusive catalytic activity of vertebrate class IIa histone deacetylases. Bioorg Med Chem Lett, 2008,18(6):1814-1819.
[5]	Duan BY, Ye D, Zhu SC, Jia WW, Lu CQ, Wang GY, Guo XD, Yu YY, Wu CY, Kang JH . HDAC10 promotes angiogenesis in endothelial cells through the PTPN22/ ERK axis. Oncotarget, 2017,8(37):61338-61349.
[6]	Houtkooper RH, Pirinen E, Auwerx J . Sirtuins as regulators of metabolism and healthspan. Nat Rev Mol Cell Biol, 2012,13(4):225-238.
[7]	Cao J, Sun L, Aramsangtienchai P, Spiegelman NA, Zhang XY, Seto E, Lin HN . DAC11 regulates type I interferon signaling through defatty-acylation of SHMT2. Proc Natl Acad Sci USA, 2019,116(12):5487-5492.
[8]	Morales CR, Li DL, Pedrozo Z, May HI, Jiang N, Kyrychenko V, Cho GW, Kim SY, Wang ZV, Rotter D, Rothermel BA, Schneider JW, Lavandero S, Gillette TG, Hill JA. Inhibition of class I histone deacetylases blunts cardiac hypertrophy through TSC2-dependent mTOR repression. Sci Signal, 2016, 9(422): ra34.
[9]	Lagger G, O'Carroll D, Rembold M, Khier H, Tischler J, Weitzer G, Schuettengruber B, Hauser C, Brunmeir R, Jenuwein T, Seiser C . Essential function of histone deacetylase 1 in proliferation control and CDK inhibitor repression. EMBO J, 2002,21(11):2672-2681.
[10]	Yang XJ, Seto E . Collaborative spirit of histone deacetylases in regulating chromatin structure and gene expression. Curr Opin Genet Dev, 2003,13(2):143-153.
[11]	Kesherwani V, Nandi SS, Sharawat SK, Shahshahan HR, Mishra PK . Hydrogen sulfide mitigates homocysteine- mediated pathological remodeling by inducing miR-133a in cardiomyocytes. Mol Cell Biochem, 2015,404(1-2):241-250.
[12]	Chandrasekaran S, Peterson RE, Mani SK, Addy B, Buchholz AL, Xu L, Thiyagarajan T, Kasiganesan H, Kern CB, Menick DR . Histone deacetylases facilitate sodium/ calcium exchanger up-regulation in adult cardiomyocytes. FASEB J, 2009,23(11):3851-3864.
[13]	Montgomery RL, Davis CA, Potthoff MJ, Haberland M, Fielitz J, Qi XX, Hill JA, Richardson JA, Olson EN . Histone deacetylases 1 and 2 redundantly regulate cardiac morphogenesis, growth, and contractility. Genes Dev, 2007,21(14):1790-1802.
[14]	Yuan YG, Peng WZ, Liu YX, Xu ZS . Palmatine attenuates isoproterenol-induced pathological hypertrophy via selectively inhibiting HDAC2 in rats. Int J Immunopathol Pharmacol, 2017,30(4):406-412.
[15]	Trivedi CM, Luo Y, Yin Z, Zhang MZ, Zhu WT, Wang T, Floss T, Goettlicher M, Noppinger PR, Wurst W, Ferrari VA, Abrams CS, Gruber PJ, Epstein JA . Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3β activity. Nat Med, 2007,13(3):324-331.
[16]	Eom GH, Kook H . Role of histone deacetylase 2 and its posttranslational modifications in cardiac hypertrophy. BMB Rep, 2015,48(3):131-138.
[17]	Raghunathan S, Goyal RK, Patel BM . Selective inhibition of HDAC2 by magnesium valproate attenuates cardiac hypertrophy. Can J Physiol Pharmacol, 2017,95(3):260-267.
[18]	Kook H, Lepore JJ, Gitler AD, Lu MM, Wing-Man Yung W, Mackay J, Zhou R, Ferrari V, Gruber P, Epstein JA . Cardiac hypertrophy and histone deacetylase-dependent transcriptional repression mediated by the atypical homeodomain protein Hop. J Clin Invest, 2003,112(6):863-871.
[19]	Trivedi CM, Zhu W, Wang Q, Jia C, Kee HJ, Li L, Hannenhalli S, Epstein JA . Hopx and Hdac2 interact to modulate Gata4 acetylation and embryonic cardiac myocyte proliferation. Dev Cell, 2010,19(3):450-459.
[20]	Li RF, Cao SS, Fang WJ, Song Y, Luo XT, Wang HY, Wang JG . Roles of HDAC2 and HDAC8 in cardiac remodeling in renovascular hypertensive rats and the effects of valproic acid sodium. Pharmacology, 2017,99(1-2):27-39.
[21]	Grégoire S, Xiao L, Nie J, Zhang X, Xu M, Li J, Wong J, Seto E, Yang XJ . Histone deacetylase 3 interacts with and deacetylates myocyte enhancer factor 2. Mol Cell Biol, 2007,27(4):1280-95.
[22]	Pillai VB, Sundaresan NR, Samant SA, Wolfgeher D, Trivedi CM, Gupta MP . Acetylation of a conserved lysine residue in the ATP binding pocket of p38 augments its kinase activity during hypertrophy of cardiomyocytes. Mol Cell Biol, 2011,31(11):2349-2363.
[23]	Trivedi CM, Lu MM, Wang QH, Epstein JA . Transgenic over-expression of Hdac3 in the heart produces increased postnatal cardiac myocyte proliferation but does not induce hypertrophy. J Biol Chem, 2008,283(39):26484-26489.
[24]	Kee HJ, Bae EH, Park S, Lee KE, Suh SH, Kim SW, Jeong MH. HDAC inhibition suppresses cardiac hypertrophy and fibrosis in DOCA-salt hypertensive rats via regulation of HDAC6/HDAC8 enzyme activity. Kidney Blood Press Res, 2013,37(4-5):229-239.
[25]	Yan MW, Chen C, Gong W, Yin ZW, Zhou L, Chaugai S, Wang DW. miR-21-3p regulates cardiac hypertrophic response by targeting histone deacetylase-8. Cardiovasc Res, 2015,105(3):340-352.
[26]	Backs J, Backs T, Bezprozvannaya S, McKinsey TA, Olson EN. Histone deacetylase 5 acquires calcium/calmodulin- dependent kinase II responsiveness by oligomerization with histone deacetylase 4. Mol Cell Biol, 2008,28(10):3437-3445.
[27]	Backs J, Worst BC, Lehmann LH, Patrick DM, Jebessa Z, Kreusser MM, Sun Q, Chen L, Heft C, Katus HA, Olson EN . Selective repression of MEF2 activity by PKA- dependent proteolysis of HDAC4. J Cell Biol, 2011,195(3):403-415.
[28]	Sucharov CC, Dockstader K, McKinsey TA. YY1 protects cardiac myocytes from pathologic hypertrophy by interacting with HDAC5. Mol Biol Cell, 2008,19(10):4141-4153.
[29]	Eom GH, Nam YS, Oh JG, Choe N, Min HK, Yoo EK, Kang G, Nguyen VH, Min JJ, Kim JK, Lee IK, Bassel- Duby R, Olson EN, Park WJ, Kook H . Regulation of acetylation of histone deacetylase 2 by p300/CBP-Associated Factor/Histone deacetylase 5 in the development of cardiac hypertrophy. Circ Res, 2014,114(7):1133-1143.
[30]	Hu T, Schreiter FC, Bagchi RA, Tatman PD, Hannink M , McKinsey TA. HDAC5 catalytic activity suppresses cardiomyocyte oxidative stress and NRF2 target gene expression. J Biol Chem, 2019,294(21):8640-8652.
[31]	Zhang H, Shao Z, Alibin CP, Acosta C, Anderson HD . Liganded peroxisome proliferator-activated receptors (ppars) preserve nuclear histone deacetylase 5 levels in endothelin-treated sprague-dawley rat cardiac myocytes. PLoS One, 2014,9(12):e115258.
[32]	Haworth RS, Stathopoulou K, Candasamy AJ, Avkiran M . Neurohormonal regulation of cardiac histone deacetylase 5 nuclear localization by phosphorylation-dependent and phosphorylation-independent mechanisms. Circ Res, 2012,110(12):1585-1595.
[33]	Zhang LL, Deng MK, Lu AH, Chen YT, Chen Y, Wu C, Tan Z, Boini KM, Yang TX, Zhu Q, Wang L . Sodium butyrate attenuates angiotensin II-induced cardiac hypertrophy by inhibiting COX2/PGE2 pathway via a HDAC5/HDAC6-dependent mechanism. J Cell Mol Med, 2019,23(12):8139-8150.
[34]	Zhang CL, McKinsey TA, Chang S, Antos CL, Hill JA, Olson EN, . Class II histone deacetylases act as signal- responsive repressors of cardiac hypertrophy. Cell, 2002,110(4):479-488.
[35]	Zhang CL, McKinsey TA, Olson EN. The transcriptional corepressor MITR is a signal-responsive inhibitor of myogenesis. Proc Natl Acad Sci USA, 2001,98(13):7354-7359.
[36]	Kee HJ, Bae EH, Park S, Lee KE, Suh SH, Kim SW, Jeong MH. HDAC inhibition suppresses cardiac hypertrophy and fibrosis in DOCA-salt hypertensive rats via regulation of HDAC6/HDAC8 enzyme activity. Kidney Blood Press Res, 2013,37(4-5):229-239.
[37]	Demos-Davies KM, Ferguson BS, Cavasin MA, Mahaffey JH, Williams SM, Spiltoir JI, Schuetze KB, Horn TR, Chen B, Ferrara C, Scellini B, Piroddi N, Tesi C, Poggesi C, Jeong MY, McKinsey TA. HDAC6 contributes to pathological responses of heart and skeletal muscle to chronic angiotensin-II signaling. Am J Physiol Heart Circ Physiol, 2014,307(2):H252-258.
[38]	Ma S, Feng J, Zhang R, Chen JW, Han D, Li X, Yang B, Li XJ, Fan MM, Li CY, Tian ZH, Wang YB, Cao F . SIRT1 activation by resveratrol alleviates cardiac dysfunction via mitochondrial regulation in diabetic cardiomyopathy mice. Oxid Med Cell Longev, 2017,2017:4602715.
[39]	Sundaresan NR, Pillai VB, Wolfgeher D, Samant S, Vasudevan P, Parekh V, Raghuraman H, Cunningham JM, Gupta M, Gupta MP. The deacetylase sirt1 promotes membrane localization and activation of akt and pdk1 during tumorigenesis and cardiac hypertrophy. Sci Signal, 2011, 4(182): ra46.
[40]	Li JY, Huang JY, Lu J, Guo Z, Li ZM, Gao H, Wang PX, Luo WW, Cai SD, Hu YH, Guo KT, Wang LP, Li ZZ, Wang MH, Zhang XL, Liu PQ . Sirtuin 1 represses PKC-ζ activity through regulating interplay of acetylation and phosphorylation in cardiac hypertrophy. Br J Pharmacol, 2019,176(3):416-435.
[41]	Li ST, Zhu ZX, Xue M, Yi XC, Liang JJ, Niu C, Chen G, Shen YJ, Zhang HP, Zheng JY, Zhao CC, Liang YZ, Cong WT, Wang Y, Jin LT . Fibroblast growth factor 21 protects the heart from angiotensin II-induced cardiac hypertrophy and dysfunction via SIRT1. Biochim Biophys Acta Mol Basis Dis, 2019,1865(6):1241-1252.
[42]	Tang XQ, Chen XF, Wang NY, Wang XM, Liang ST, Zheng W, Lu YB, Zhao X, Hao DL, Zhang ZQ, Zou MH, Liu DP, Chen HZ . SIRT2 acts as a cardioprotective deacetylase in pathological cardiac hypertrophy. Circulation, 2017,136(21):2051-2067.
[43]	Pillai VB, Bindu S, Sharp W, Fang YH, Kim G, Gupta M, Samant S, Gupta MP . Sirt3 protects mitochondrial DNA damage and blocks the development of doxorubicin- induced cardiomyopathy in mice. Am J Physiol Heart Circ Physiol, 2016,310(8):H962-972.
[44]	Sundaresan NR, Gupta M, Kim G, Rajamohan SB, Isbatan A, Gupta MP . Sirt3 blocks the cardiac hypertrophic response by augmenting foxo3a-dependent antioxidant defense mechanisms in mice. J Clin Invest, 2009,119(9):2758-2771.
[45]	Pillai VB, Sundaresan NR, Kim G, Gupta M, Rajamohan SB, Pillai JB, Samant S, Ravindra PV, Isbatan A, Gupta MP . Exogenous nad blocks cardiac hypertrophic response via activation of the sirt3-lkb1-amp-activated kinase pathway. J Biol Chem, 2010,285(5):3133-3144.
[46]	Luo YX, Tang XQ, An XZ, Xie XM, Chen XF, Zhao X, Hao DL, Chen HZ, Liu DP . SIRT4 accelerates Ang II-induced pathological cardiac hypertrophy by inhibiting manganese superoxide dismutase activity. Eur Heart J, 2017,38(18):1389-1398.
[47]	Sadhukhan S, Liu XJ, Ryu D, Nelson OD, Stupinski JA, Li Z, Chen W, Zhang S, Weiss RS, Locasale JW, Auwerx J, Lin HN . Metabolomics-assisted proteomics identifies succinylation and SIRT5 as important regulators of cardiac function. Proc Natl Acad Sci USA, 2016,113(16):4320-4325.
[48]	Hershberger KA, Abraham DM, Martin AS, Mao L, Liu J, Gu H, Locasale JW, Hirschey MD . Sirtuin 5 is required for mouse survival in response to cardiac pressure overload. J Biol Chem, 2017,292(48):19767-19781.
[49]	Sundaresan NR, Vasudevan P, Zhong L, Kim G, Samant S, Parekh V, Pillai VB, Ravindra PV, Gupta M, Jeevanandam V, Cunningham JM, Deng CX, Lombard DB, Mostoslavsky R, Gupta MP . The sirtuin sirt6 blocks igf-akt signaling and development of cardiac hypertrophy by targeting c-jun. Nat Med, 2012,18(11):1643-1650.
[50]	Yamamura S, Izumiya Y, Araki S, Nakamura T, Kimura Y, Hanatani S, Yamada T, Ishida T, Yamamoto M, Onoue Y, Arima Y, Yamamoto E, Sunagawa Y, Yoshizawa T, Nakagata N, Bober E, Braun T, Sakamoto K, Kaikita K, Morimoto T, Yamagata K, Tsujita K. Cardiomyocyte Sirt(Sirtuin) 7 ameliorates stress-induced cardiac hypertrophy by interacting with and deacetylating GATA4. Hypertension, 2020,75(1):98-108.
[51]	Schueler M, Zhang Q, Schlesinger J, Tönjes M, Sperling SR . Dynamics of Srf, p300 and histone modifications during cardiac maturation in mouse. Mol Biosyst, 2012,8(2):495-503.
[52]	Schlesinger J, Schueler M, Grunert M, Fischer JJ, Zhang Q, Krueger T, Lange M, Tönjes M, Dunkel I, Sperling SR . The cardiac transcription network modulated by Gata4, Mef2a, Nkx2.5, Srf, histone modifications, and microRNAs. PLoS Genet, 2011,7(2):e1001313.
[53]	Mathias RA, Guise AJ, Cristea IM . Post-translational modifications regulate class IIa histone deacetylase (HDAC) function in health and disease. Mol Cell Proteomics, 2015,14(3):456-470.
[54]	Vega RB, Harrison BC, Meadows E, Roberts CR, Papst PJ, Olson EN , McKinsey TA. Protein kinases C and D mediate agonist-dependent cardiac hypertrophy through nuclear export of histone deacetylase 5. Mol Cell Biol, 2004,24(19):8374-8385.
[55]	McKinsey TA, Zhang CL, Lu J, Olson EN . Signal-dependent nuclear export of a histone deacetylase regulates muscle differentiation. Nature, 2000,408(6808):106-111.
[56]	Sparrow DB, Miska EA, Langley E, Reynaud-Deonauth S, Kotecha S, Towers N, Spohr G, Kouzarides T, Mohun TJ . MEF-2 function is modified by a novel co-repressor, MITR. EMBO J, 1999,18(18):5085-5098.
[57]	Morin S1, Charron F, Robitaille L, Nemer M . GATA- dependent recruitment of MEF2 proteins to target promoters. EMBO J, 2000,19(9):2046-2055.
[58]	Youn HD, Chatila TA, Liu JO . Integration of calcineurin and MEF2 signals by the coactivator p300 during T-cell apoptosis. EMBO J, 2000,19(16):4323-4331.
[59]	Zhang M, Hagenmueller M, Riffel JH, Kreusser MM, Bernhold E, Fan J, Katus HA, Backs J, Hardt SE . Calcium/Calmodulin-dependent protein kinase II couples Wnt signaling with histone deacetylase 4 and mediates dishevelled-induced cardiomyopathy. Hypertension, 2015,65(2):335-344.
[60]	Calalb MB, McKinsey TA, Newkirk S, Huynh K, Sucharov CC, Bristow MR. Increased phosphorylation- dependent nuclear export of class II histone deacetylases in failing human heart. Clin Transl Sci, 2009,2(5):325-332.
[61]	Cao DS, Wang ZG, Zhang CL, Oh J, Xing W, Li S, Richardson JA, Wang DZ, Olson EN . Modulation of smooth muscle gene expression by association of histone acetyltransferases and deacetylases with myocardin. Mol Cell Biol, 2005,25(1):364-376.
[62]	McDonald OG, Wamhoff BR, Hoofnagle MH, Owens GK . Control of SRF binding to CArG box chromatin regulates smooth muscle gene expression in vivo. J Clin Invest, 2006,116(1):36-48.
[63]	Fischle W, Dequiedt F, Hendzel MJ, Guenther MG, Lazar MA, Voelter W, Verdin E . Enzymatic activity associated with class II HDACs is dependent on a multiprotein complex containing HDAC3 and SMRT/N-CoR. Mol Cell, 2002,9(1):45-57.
[64]	Chang CW, Lee L, Yu D, Dao K, Bossuyt J, Bers DM . Acute β-adrenergic activation triggers nuclear import of histone deacetylase 5 and delays G(q)-induced transcriptional activation. J Biol Chem, 2013,288(1):192-204.
[65]	Mangmool S, Shukla AK, Rockman HA . β-arrestin- dependent activation of Ca ²+/Calmodulin kinase Ⅱ after β-adrenergic receptor stimulation . J Cell Biol, 2010,189(3):573-587.
[66]	Gurha P, Abreu-Goodger C, Wang T, Ramirez MO, AL, van Drumond S, Chen Dongen Y, Bartonicek N, Enright AJ, Lee B, Kelm RJ Jr, Reddy AK, Taffet GE, Bradley A, Wehrens XH, Entman ML, Rodriguez A,. Targeted deletion of microRNA-22 promotes stress-induced cardiac dilation and contractile dysfunction. Circulation, 2012,125(22):2751-2761.
[67]	Huang ZP, Chen JH, Seok HY, Zhang Z, Kataoka M, Hu XY, Wang DZ . MicroRNA-22 regulates cardiac hypertrophy and remodeling in response to stress. Circ Res, 2013,112(9):1234-1243.
[68]	Diniz GP, Lino CA, Moreno CR, Senger N, Barreto-Chaves MLM . MicroRNA-1 overexpression blunts cardiomyocyte hypertrophy elicited by thyroid hormone. J Cell Physiol, 2017,232(12):3360-3368.
[69]	Xiao Y, Zhang X, Fan S, Cui G, Shen Z . MicroRNA-497 inhibits cardiac hypertrophy by targeting Sirt4. PLoS One, 2016,11(12):e0168078.
[70]	Kee HJ, Sohn IS, Nam KI, Park JE, Qian YR, Yin Z, Ahn Y, Jeong MH, Bang YJ, Kim N, Kim JK, Kim KK, Epstein JA, Kook H . Inhibition of histone deacetylation blocks cardiac hypertrophy induced by angiotensin II infusion and aortic banding. Circulation, 2006,113(1):51-59.
[71]	Cao DJ, Wang ZV, Battiprolu PK, Jiang N, Morales CR, Kong Y, Rothermel BA, Gillette TG, Hill JA . Histone deacetylase (HDAC) inhibitors attenuate cardiac hypertrophy by suppressing autophagy. Proc Natl Acad Sci USA, 2011,108(10):4123-4128.
[72]	Antos CL, McKinsey TA, Dreitz M, Hollingsworth LM, Zhang CL, Schreiber K, Rindt H, Gorczynski RJ, Olson EN. Dose-dependent blockade to cardiomyocyte hypertrophy by histone deacetylase inhibitors. J Biol Chem, 2003,278(31):28930-28937.
[73]	Majumdar G, Adris P, Bhargava N, Chen H, Raghow R . Pan-histone deacetylase inhibitors regulate signaling pathways involved in proliferative and pro-inflammatory mechanisms in H9c2 cells. BMC Genomics, 2012,13:709.
[74]	Majumdar G, Rooney RJ, Johnson IM, Raghow R . Panhistone deacetylase inhibitors inhibit proinflammatory signaling pathways to ameliorate interleukin-18-induced cardiac hypertrophy. Physiol Genomics, 2011,43(24):1319-1333.
[75]	Kook H, Lepore JJ, Gitler AD, Lu MM, Wing-Man Yung W, Mackay J, Zhou R, Ferrari V, Gruber P, Epstein JA. Cardiac hypertrophy and histone deacetylase-dependent transcriptional repression mediated by the atypical homeodomain protein Hop. J Clin Invest, 2003,112(6):863-871.
[76]	Kong YQ, Tannous P, Lu GR, Berenji K, Rothermel BA, Olson EN, Hill JA . Suppression of class I and II histone deacetylases blunts pressure-overload cardiac hypertrophy. Circulation, 2006,113(22):2579-2588.
[77]	Iyer A, Fenning A, Lim J, Le GT, Reid RC, Halili MA, Fairlie DP, Brown L . Antifibrotic activity of an inhibitor of histone deacetylases in DOCA-salt hypertensive rats. Br J Pharmacol, 2010,159(7):1408-1417.
[78]	Kang SH, Seok YM, Song MJ, Lee HA, Kurz T, Kim I . Histone deacetylase inhibition attenuates cardiac hypertrophy and fibrosis through acetylation of mineralocorticoid receptor in spontaneously hypertensive rats. Mol Pharmacol, 2015,87(5):782-791.
[79]	Cho YK, Eom GH, Kee HJ, Kim HS, Choi WY, Nam KI, Ma JS, Kook H . Sodium valproate, a histone deacetylase inhibitor, but not captopril, prevents right ventricular hypertrophy in rats. Circ J, 2010,74(4):760-770.
[80]	Cardinale JP, Sriramula S, Pariaut R, Guggilam A, Mariappan N, Elks CM, Francis J . HDAC inhibition attenuates inflammatory, hypertrophic, and hypertensive responses in spontaneously hypertensive rats. Hypertension, 2010,56(3):437-444.
[81]	Gallo P, Latronico MV, Gallo P, Grimaldi S, Borgia F, Todaro M, Jones P, Gallinari P, De Francesco R, Ciliberto G, Steinkühler C, Esposito G, Condorelli G . Inhibition of class I histone deacetylase with an apicidin derivative prevents cardiac hypertrophy and failure. Cardiovasc Res, 2008,80(3):416-424.
[82]	Ooi JY, Tuano NK, Rafehi H, Gao XM, Ziemann M, Du XJ, El-Osta A . HDAC inhibition attenuates cardiac hypertrophy by acetylation and deacetylation of target genes. Epigenetics, 2015,10(5):418-430.
[83]	Cao JH, Liao WT, Wo C, Xu GR, Xu HX, Li PL, Tao Y, Wang P, Lin JR, Deng LR . Transcriptome screening and verification of genes related to metabolism affected by histone deacetylase inhibitors. Hereditas(Beijing), 2015,37(9):918-925.
	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]

组蛋白去乙酰化酶在调节心肌肥大过程中的作用机制

The mechanism underlying histone deacetylases regulating cardiac hypertrophy

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