SIRT3与细胞代谢及心血管疾病的相关性

doi:10.16288/j.yczz.14-283

遗传 ›› 2015, Vol. 37 ›› Issue (2): 111-120.doi: 10.16288/j.yczz.14-283

• 综述 • 下一篇

SIRT3与细胞代谢及心血管疾病的相关性

曹丽娟,刘昕訸,查晴,宋倩,杨克,刘艳

上海交通大学医学院附属瑞金医院心血管内科,上海 200025

收稿日期:2014-08-26 出版日期:2015-02-20 发布日期:2015-01-19
通讯作者: 刘艳,博士,主任医师,硕士生导师,研究方向：动脉粥样硬化。E-mail：liuyan_ivy@126.com
作者简介:曹丽娟,硕士研究生,专业方向：动脉粥样硬化。Tel：021-64370045;E-mail：caolijuanqq@163.com
基金资助:
国家自然科学基金项目(编号：81200204,81470547)资助

The relationship of SIRT3 with cellular metabolism and cardiovascular diseases

Lijuan Cao,Xinhe Liu,Qing Zha,Qian Song,Ke Yang,Yan Liu

Department of Cardiology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China

Received:2014-08-26 Online:2015-02-20 Published:2015-01-19

摘要/Abstract

摘要： 蛋白去乙酰化酶在细胞生理过程中发挥着极为重要的作用。人蛋白去乙酰化酶包括HDACⅠ、HDACⅡ、HDACⅢ和HDACⅣ4个家族。其中第Ⅲ类即Sir2(Silent information regulator 2)家族包括7个成员——SIRT1~ SIRT7,每个成员都具有不同的细胞定位,并且发挥不同的生物学功能。作为主要定位于线粒体的组蛋白去乙酰化酶,SIRT3不仅调节细胞的能量代谢,并在细胞凋亡、肿瘤生长和一些疾病中发挥作用。文章综述了SIRT3在细胞代谢中的生物学功能以及其在心血管疾病中的研究进展。

关键词: SIRT3, 组蛋白去乙酰化酶, 细胞代谢, 心血管疾病

Abstract: Protein deacetylases play an extremely crucial role in cellular biological processes and have been categorized into four families (HDACⅠ, HDACⅡ, HDACⅢ and HDACⅣ) in human. Of them, HDACⅢ, also known as the Sir2 (Silent information regulator 2) family, contains seven members, SIRT1-7, each exhibiting different cellular localization and biological function. As a major mitochondrial deacetylase, SIRT3 not only modulates cellular metabolism, but also plays important roles in apoptosis, tumor growth, aging and a number of other diseases. In this review, we summarize recent findings related to SIRT3 with an emphasis on its biological functions in regulating cell metabolism and its possible roles in cardiovascular diseases.

Key words: SIRT3, HDAC, cell metabolism, cardiovascular diseases

曹丽娟,刘昕訸,查晴,宋倩,杨克,刘艳. SIRT3与细胞代谢及心血管疾病的相关性[J]. 遗传, 2015, 37(2): 111-120.

Lijuan Cao,Xinhe Liu,Qing Zha,Qian Song,Ke Yang,Yan Liu. The relationship of SIRT3 with cellular metabolism and cardiovascular diseases[J]. HEREDITAS(Beijing), 2015, 37(2): 111-120.

参考文献

[1] Gregoretti IV, Lee YM, Goodson HV. Molecular evolution of the histone deacetylase family: functional implications of phylogenetic analysis. J Mol Biol , 2004, 338(1): 17-31.
[2] Yang XJ, Seto E. The Rpd3/Hda1 family of lysine deacetylases: from bacteria and yeast to mice and men. Nat Rev Mol Cell Biol , 2008, 9(3): 206-218.
[3] Zhang T, Kohlhaas M, Backs J, Mishra S, Phillips W, Dybkova N, Chang SR, Ling HY, Bers DM, Maier LS, Olson EN, Brown JH. CaMKIIδ isoforms differentially affect calcium handling but similarly regulate HDAC/MEF2 transcriptional responses. J Biol Chem , 2007, 282(48): 35078-35087.
[4] Nebbioso A, Manzo F, Miceli M, Conte M, Manente L, Baldi A, De Luca A, Rotili D, Valente S, Mai A, Usiello A, Gronemeyer H, Altucci L. Selective classⅡ HDAC inhibitors impair myogenesis by modulating the stability and activity of HDAC-MEF2 complexes. EMBO Rep , 2009, 10(7): 776-782.
[5] Lu J, McKinsey TA, Zhang CL, Olson EN. Regulation of skeletal myogenesis by association of the MEF2 transcription factor with class Ⅱ histone deacetylases. Mol Cell , 2000, 6(2): 233-244.
[6] Schwer B, North BJ, Frye RA, Ott M, Verdin E. The human silent information regulator (Sir)2 homologue hSIRT3 is a mitochondrial nicotinamide adenine dinucleotide-dependent deacetylase. J Cell Biol , 2002, 158(4): 647-657.
[7] Kendrick AA, Choudhury M, Rahman SM, McCurdy CE, Friederich M, Van Hove JL, Watson PA, Birdsey N, Bao J, Gius D, Sack MN, Jing E, Kahn CR, Friedman JE, Jonscher KR. Fatty liver is associated with reduced SIRT3 activity and mitochondrial protein hyperacetylation. Biochem J , 2011, 433(3): 505-514.
[8] Yang YJ, Cimen H, Han MJ, Shi T, Deng JH, Koc H, Palacios OM, Montier L, Bai YD, Tong Q, Koc EC. NAD + -dependent deacetylase SIRT3 regulates mitochondrial protein synthesis by deacetylation of the ribosomal protein MRPL10. J Biol Chem , 2010, 285(10): 7417-7429.
[9] Kim SH, Lu HF, Alano CC. Neuronal Sirt3 protects against excitotoxic injury in mouse cortical neuron culture. PLoS One , 2011, 6(3): e14731.
[10] Onyango P, Celic I, McCaffery JM, Boeke JD, Feinberg AP. SIRT3, a human SIR2 homologue, is an NAD-dependent deacetylase localized to mitochondria. Proc Natl Acad Sci USA , 2002, 99(21): 13653-13658.
[11] Jin L, Wei WT, Jiang YB, Peng H, Cai JH, Mao C, Dai H, Choy W, Bemis JE, Jirousek MR, Milne JC, Westphal CH, Perni RB. Crystal structures of human SIRT3 displaying substrate-induced conformational changes. J Biol Chem , 2009, 284(36): 24394-24405.
[12] Bao J, Lu Z, Joseph JJ, Carabenciov D, Dimond CC, Pang L, Samsel L, McCoy JP Jr, Leclerc J, Nguyen P, Gius D, Sack MN. Characterization of the murine SIRT3 mitochondrial localization sequence and comparison of mitochondrial enrichment and deacetylase activity of long and short SIRT3 isoforms. J Cell Biochem , 2010, 110(1): 238-247.
[13] Buler M, Aatsinki SM, Izzi V, Uusimaa J, Hakkola J. SIRT5 is under the control of PGC-1α and AMPK and is involved in regulation of mitochondrial energy metabolism. FASEB J , 2014, 28(7): 3225-3237.
[14] Das S, Mitrovsky G, Vasanthi HR, Das DK. Antiaging properties of a grape-derived antioxidant are regulated by mitochondrial balance of fusion and fission leading to mitophagy triggered by a signaling network of Sirt1-Sirt3- Foxo3-PINK1-PARKIN. Oxid Med Cell Longev , 2014, 2014: Article ID 345105.
[15] Dolle C, Rack JG, Ziegler M. NAD and ADP-ribose metabolism in mitochondria. FEBS J , 2013, 280(15): 3530-3541.
[16] Du G, Song YL, Zhang T, Ma L, Bian N, Chen XM, Feng JY, Chang Q, Li ZC. Simvastatin attenuates TNF-α-induced apoptosis in endothelial progenitor cells via the upregulation of SIRT1. Int J Mol Med , 2014, 34(1): 177-182.
[17] Fernandez-Marcos PJ, Jeninga EH, Canto C, Harach T, de Boer VC, Andreux P, Moullan N, Pirinen E, Yamamoto H, Houten SM, Schoonjans K, Auwerx J. Muscle or liver-specific Sirt3 deficiency induces hyperacetylation of

编辑推荐

Metrics

www.chinagene.cn
备案号：京ICP备09063187号-4
总访问:,今日访问:,当前在线:

SIRT3与细胞代谢及心血管疾病的相关性

The relationship of SIRT3 with cellular metabolism and cardiovascular diseases

PDF (PC)

可视化

被引次数

摘要/Abstract

引用本文

使用本文

参考文献

相关文章 7

编辑推荐

Metrics

[1]	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.
[2]	孙兆庆, 闫波. 转录因子GATA6在心血管疾病中的作用及其调控机制[J]. 遗传, 2019, 41(5): 375-383.
[3]	王永煜,余薇,周斌. Hippo信号通路与心血管发育及疾病调控[J]. 遗传, 2017, 39(7): 576-587.
[4]	李建辉, 汪春付, 白帆, 庄严, 毛卓君, 孙永涛. 流式细胞术检测组蛋白乙酰化水平方法的建立与应用[J]. 遗传, 2016, 38(6): 581-587.
[5]	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[J]. 遗传, 2015, 37(9): 918-925.
[6]	马尚耀，董政福，成慧娟. 浅谈干扰素（及其诱导物poly 1:C)抗病毒作用的分子基基础[J]. 遗传, 2003, 4(5): 567-572.
[7]	李晓雪，陆军，罗巅辉，黄百渠. 组蛋白去乙酰化酶SIR2与染色质沉默[J]. 遗传, 2003, 25(4): 484-488.