我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

线粒体蛋白质组学在心血管疾病中的改变及意义

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2015年第4期
页码:
474-479
栏目:
综述
出版日期:
2015-04-20

文章信息/Info

Title:
Changes of mitochondrial proteome in cardiovascular disease
作者:
李畑波; 蹇 朝; 肖颖彬
(第三军医大学新桥医院全军心血管外科研究所，重庆 400037)
Author(s):
LI Tian-bo;  JIAN Zhao;  XIAO Ying-bin
(Institute of Cardiovascular Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China)
关键词:
线粒体; 蛋白质组学; 心血管疾病
Keywords:
mitochondria;  proteome;  cardiovascular disease
分类号:
R54
DOI:
-
文献标识码:
A
摘要:
线粒体产生的ATP是细胞能量的来源，线粒体是包含约1 000种蛋白质的最重要的细胞器之一。这些蛋白形成线粒体蛋白质功能网（mitochondrial protein functional network），在细胞能量代谢、脂肪酸代谢、细胞信号传导、细胞凋亡与自噬等途径中发挥着重要作用。另外，线粒体功能失调与多种心血管疾病的发生、发展密切相关，线粒体蛋白质组在其中扮演了不可缺少的角色。本文综述线粒体蛋白组学在常见心血管疾病中的研究进展及其意义。
Abstract:
Mitochondria, containing ~1 000 different proteins, are the source of energy for a cell and are one of the most complex subcellular organelles. The proteins forming the functional mitochondrial network play indispensable roles in energy production, fatty acid metabolism, cell signaling, cell apoptosis and autophagy. Mitochondrial dysfunction is closely related to the occurrence and progression of cardiovascular disease. In this article we focus on the cardiac mitochondrial proteome, with emphasis on the changes associated with cardiovascular disease.

参考文献/References

[1]Lane N,Martin W.The energetics of genome complexity[J].Nature,2010,467(7318):929-934.
[2]SHeazlewood JL,Tonti-Filippini JS,Gout AM,et al.Experimental analysis of the Arabidopsis mitochondrial proteome highlights signaling and regulatory components, provides assessment of targeting prediction programs, and indicates plant-specific mitochondrial proteins[J].Plant Cell,2004,16(1):241-256.
[3]Reinders J,Zahedi RP,Pfanner N,et al.Toward the complete yeast mitochondrial proteome:multidimensional separation techniques for mitochondrial proteomics[J].J Proteome Res,2006,5(7):1543-1554.
[4]Smith DG,Gawryluk RM,Spencer DF,et al.Exploring the mitochondrial proteome of the ciliate protozoon Tetrahymena thermophila:direct analysis by tandem mass spectrometry[J].J Mol Biol,2007,374(3):837-863.
[5]Pagliarini DJ,Calvo SE,Chang B,et al.A mitochondrial protein compendium elucidates complex I disease biology[J].Cell,2008,134(1):112-123.
[6]Calvo SE,Mootha VK.The mitochondrial proteome and human disease[J].Annu Rev Genomics Hum Genet,2010,11:25-44.
[7]Dimauro S,Schon EA.Mitochondrial respiratory-chain diseases[J].N Engl J Med,2003,348(26):2656-2668.
[8]Johnson DT,Harris RA,French S,et al.Tissue heterogeneity of the mammalian mitochondrial proteome[J].Am J Physiol Cell Physiol,2007,292(2):C689-C697.
[9]Lotz C,Lin AJ,Black CM,et al.Characterization,design, and function of the mitochondrial proteome: from organs to organisms[J].J Proteome Res,2014,13(2):433-446.
[10]Taylor SW,Fahy E,Murray J,et al.Oxidative post-translational modification of tryptophan residues in cardiac mitochondrial proteins[J].J Biol Chem,2003,278(22):19587-19590.
[11]Taylor SW,Fahy E,Zhang B,et al.Characterization of the human heart mitochondrial proteome[J].Nat Biotechnol,2003,21(3):281-286.
[12]Taylor SW,Warnock DE,Glenn GM,et al.An alternative strategy to determine the mitochondrial proteome using sucrose gradient fractionation and 1D PAGE on highly purified human heart mitochondria[J].J Proteome Res,2003,1(5):451-458.
[13]Gibson BW.The human mitochondrial proteome:oxidative stress, protein modifications and oxidative phosphorylation[J].Int J Biochem Cell Biol,2005,37(5):927-934.
[14]Viganò A,Vasso M,Caretti A,et al.Protein modulation in mouse heart under acute and chronic hypoxia[J].Proteomics,2011,11(21):4202-4217.
[15]Zhu WZ,Wu XF,Zhang Y,et al.Proteomic analysis of mitochondrial proteins in cardiomyocytes from rats subjected to intermittent hypoxia[J].Eur J Appl Physiol,2012,112(3):1037-1046.
[16]Hollander JM,Baseler WA,Dabkowski ER.Proteomic remodeling of mitochondria in heart failure[J].Congest Heart Fail,2011,17(6):262-268.
[17]Osterholt M,Nguyen TD,Schwarzer M,et al.Alterations in mitochondrial function in cardiac hypertrophy and heart failure[J].Heart Fail Rev,2013,18(5):645-656.
[18]Knecht M,Regitz-Zagrosek V,Pleissner KP,et al.Characterization of myocardial protein composition in dilated cardiomyopathy by two-dimensional gel electrophoresis[J].Eur Heart J, 1994, 15(Suppl D):37-44.
[19]Hasenfuss G.Animal models of human cardiovascular disease,heart failure and hypertrophy[J]. Cardiovasc Res,1998,39(1):60-76.
[20]Bugger H,Schwarzer M,Chen D,et al.Proteomic remodelling of mitochondrial oxidative pathways in pressure overload-induced heart failure[J].Cardiovasc Res,2010,85(2):376-384.
[21]Dai DF,Hsieh EJ,Liu Y,et al.Mitochondrial proteome remodelling in pressure overload-induced heart failure: the role of mitochondrial oxidative stress[J].Cardiovasc Res,2012,93(1):79-88.
[22]Jin X,Xia L,Wang LS,et al.Differential protein expression in hypertrophic heart with and without hypertension in spontaneously hypertensive rats[J].Proteomics,2006,6(6):1948-1956.
[23]Liu T,Chen L,Kim E,et al.Mitochondrial proteome remodeling in ischemic heart failure[J].Life Sci,2014,101(1/2):27-36.
[24]Rosca MG,Vazquez EJ,Kerner J,et al.Cardiac mitochondria in heart failure:decrease in respirasomes and oxidative phosphorylation[J].Cardiovasc Res,2008,80(1):30-39.
[25]Madamanchi NR,Runge MS.Mitochondrial dysfunction in atherosclerosis[J].Circ Res,2007,100(4):460-473.
[26]Mercer JR,Cheng KK,Figg N,et al.DNA damage links mitochondrial dysfunction to atherosclerosis and the metabolic syndrome[J].Circ Res,2010,107(8):1021-1031.
[27]Viiri LE,Full LE,Navin TJ,et al.Smooth muscle cells in human atherosclerosis:proteomic profiling reveals differences in expression of Annexin A1 and mitochondrial proteins in carotid disease[J].J Mol Cell Cardiol,2013,54:65-72.
[28]Buerke M,Schwertz H,L?ngin T,et al.Proteome analysis of myocardial tissue following ischemia and reperfusion--effects of complement inhibition[J]. Biochim Biophys Acta,2006,1764(10):1536-1545.
[29]Ballinger SW.Mitochondrial dysfunction in cardiovascular disease[J].Free Radic Biol Med,2005,38(10):1278-1295.

备注/Memo

备注/Memo:
收稿日期：2014-07-18.
基金项目：国家自然科学基金面上项目资助(81270228)
通讯作者：肖颖彬，主任医师，主要从事心肌慢性缺氧适应研究 Email：xiaoyb@vipsina.com
作者简介：李畑波，硕士生 Email： cqlitianbo@qq.com
更新日期/Last Update: 2015-04-22