线粒体功能障碍与心房颤动

刘彤; 张晓伟

doi:10.13201/j.issn.1001-1439.2016.03.001

线粒体功能障碍与心房颤动

刘彤^,,
张晓伟

- 天津市心血管病离子与分子机能重点实验室天津医科大学第二医院心脏科天津心脏病学研究所(天津, 300211)
基金项目:
国家自然科学基金资助项目(No:30900618,81270245,81570298)

详细信息

通讯作者: 刘彤,E-mail:liutongdoc@126.com

中图分类号: R541.7

收稿日期: 2016-02-02

Mitochondrial dysfunction and atrial fibrillation

LIU Tong^,,
ZHANG Xiaowei

- Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, 300211, China

More Information

Corresponding author: LIU Tong, E-mail: liutongdoc@126.com

Received Date: 02 February 2016

摘要

摘要: 心房颤动(房颤)是全球范围内最常见的持续性心律失常,其发病率随着年龄和其他心血管病危险因素的增多而升高。房颤的发生发展与心房结构重构和电重构有关,但其潜在的机制尚不完全清楚。线粒体是心脏的能量工厂,在肌质网、肌丝和T管周围形成复杂的网络系统,在细胞能量代谢、信号转导、氧化还原状态的控制以及细胞凋亡方面有重要作用。线粒体功能障碍会影响细胞膜离子通道及转运体的能量供应,导致心律失常发生。最近研究表明,线粒体功能障碍与房颤的发生发展有关。本文将探讨线粒体功能障碍与房颤的关系。
- 心房颤动 /
- 线粒体功能障碍 /
- 氧化应激 /
- 钙超载 /
- 线粒体生物合成
Abstract: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia worldwide and its incidence increases with ageing and other cardiovascular risk factors. The occurrence and development of AF is associated with atrial structural and electrical remodeling, but the potential mechanisms remain unclear. Mitochondria, energy factory in the heart, form a network surrounding sarcoplasmic reticulum, myofilaments and t-tubules, and play an important role in energy metabolism, signaling transduction, redox state control, cell apoptosis. Mitochondrial dysfunction readily disrupts the cardiac rhythm through depleting energy supply to the ion channels and transporters. Recent researches have evaluated the potential role of the mitochondrial dysfunction in the development of AF. In this review, we tend to summarize the potential relationship between mitochondrial dysfunction and atrial fibrillation.
- atrial fibrillation /
- mitochondrial dysfunction /
- oxidative stress /
- calcium overload /
- mitochondrial biogenesis

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参考文献(31)

[1]	CAMM A J,LIP G Y,DE CATERINA R,et al.2012focused update of the ESC Guidelines for the management of atrial fibrillation:an update of the 2010 ESC Guidelines for the management of atrial fibrillation-developed with the special contribution of the European Heart Rhythm Association[J].Europace,2012,14:1385-1413.
[2]	BROWN D A,O'ROURKE B.Cardiac mitochondria and arrhythmias[J].Cardiovasc Res,2010,88:241-249.
[3]	JEONG E M,LIU M,STURDY M,et al.Metabolic stress,reactive oxygen species,and arrhythmia[J].J Mol Cell Cardiol,2012,52:454-463.
[4]	AKAR F G,O'ROURKE B.Mitochondria are sources of metabolic sink and arrhythmias[J].Pharmacol Ther,2011,131:287-294.
[5]	MONTAIGNE D,MARECHAL X,LACROIX D,et al.From cardiac mitochondrial dysfunction to clinical arrhythmias[J].Int J Cardiol,2015,184:597-599.
[6]	MONTAIGNE D,MARECHAL X,LEFEBVRE P,et al.Mitochondrial dysfunction as an arrhythmogenic substrate:a translational proof-of-concept study in patients with metabolic syndrome in whom post-operative atrial fibrillation develops[J].J Am Coll Cardiol,2013,62:1466-1473.
[7]	DORN G W,2ND.Mitochondrial dynamics in heart disease[J].Biochim Biophys Acta,2013,1833:233-241.
[8]	HALL A R,BURKE N,DONGWORTH R K,et al.Mitochondrial fusion and fission proteins:novel therapeutic targets for combating cardiovascular disease[J].Br J Pharmacol,2014,171:1890-1906.
[9]	OYEWOLE A O,BIRCH-MACHIN M A.Mitochondria-targeted antioxidants[J].Faseb J,2015,29:4766-4771.
[10]	YARANA C,SRIPETCHWANDEE J,SANIT J,et al.Calcium-induced cardiac mitochondrial dysfunction is predominantly mediated by cyclosporine A-dependent mitochondrial permeability transition pore[J].Arch Med Res,2012,43:333-338.
[11]	O'ROURKE B,RAMZA B M,MARBAN E.Oscillations of membrane current and excitability driven by metabolic oscillations in heart cells[J].Science,1994,265:962-966.
[12]	ZHOU L,SOLHJOO S,MILLARE B,et al.Effects of regional mitochondrial depolarization on electrical propagation:implications for arrhythmogenesis[J].Circ Arrhythm Electrophysiol,2014,7:143-151.
[13]	OLSON T M,ALEKSEEV A E,MOREAU C,et al.KATP channel mutation confers risk for vein of Marshall adrenergic atrial fibrillation[J].Nat Clin Pract Cardiovasc Med,2007,4:110-116.
[14]	BALANA B,DOBREV D,WETTWER E,et al.Decreased ATP-sensitive K(+)current density during chronic human atrial fibrillation[J].J Mol Cell Cardiol,2003,35:1399-1405.
[15]	SEPPET E,EIMRE M,PEET N,et al.Compartmentation of energy metabolism in atrial myocardium of patients undergoing cardiac surgery[J].Mol Cell Biochem,2005,270:49-61.
[16]	TURRENS J F.Mitochondrial formation of reactive oxygen species[J].J Physiol,2003,552:335-344.
[17]	KURZ F T,DERUNGS T,AON M A,et al.Mitochondrial networks in cardiac myocytes reveal dynamic coupling behavior[J].Biophys J,2015,108:1922-1933.
[18]	LIU T,ZHAO H,LI J,et al.Rosiglitazone attenuates atrial structural remodeling and atrial fibrillation promotion in alloxan-induced diabetic rabbits[J].Cardiovasc Ther,2014,32:178-183.
[19]	POLOVINA M M,OSTOJIC M C,POTPARA T S.Relation of biomarkers of inflammation and oxidative stress with hypertension occurrence in lone atrial fibrillation[J].Mediators Inflamm,2015,2015:653026.
[20]	BUKOWSKA A,SCHILD L,KEILHOFF G,et al.Mitochondrial dysfunction and redox signaling in atrial tachyarrhythmia[J].Exp Biol Med(Maywood),2008,233:558-574.
[21]	XIE W,SANTULLI G,REIKEN S R,et al.Mitochondrial oxidative stress promotes atrial fibrillation[J].Sci Rep,2015,5:11427.
[22]	DEDKOVA E N,BLATTER L A.Calcium signaling in cardiac mitochondria[J].J Mol Cell Cardiol,2013,58:125-133.
[23]	SANTO-DOMINGO J,WIEDERKEHR A,DE MARCHI U.Modulation of the matrix redox signaling by mitochondrial Ca(2.)[J].World J Biol Chem,2015,6:310-323.
[24]	FLOREA S M,BLATTER L A.The role of mitochondria for the regulation of cardiac alternans[J].Front Physiol,2010,1:141.
[25]	YANG K C,BONINI M G,DUDLEY S C,JR.Mitochondria and arrhythmias[J].Free Radic Biol Med,2014,71:351-361.
[26]	HIONA A,SANZ A,KUJOTH G C,et al.Mitochondrial DNA mutations induce mitochondrial dysfunction,apoptosis and sarcopenia in skeletal muscle of mitochondrial DNA mutator mice[J].PLoS One,2010,5:e11468.
[27]	PARK H W,AHN Y,JEONG M H,et al.Chronic atrial fibrillation associated with somatic mitochondrial DNA mutations in human atrial tissue[J].J Clin Pathol,2007,60:948-950.
[28]	LEE J S,KO Y G,SHIN K J,et al.Mitochondrial DNA 4977bp deletion mutation in peripheral blood reflects atrial remodeling in patients with non-valvular atrial fibrillation[J].Yonsei Med J,2015,56:53-61.
[29]	KARAMANLIDIS G,GARCIA-MENENDEZ L,KOLWICZ S C,JR,et al.Promoting PGC-1alphadriven mitochondrial biogenesis is detrimental in pressure-overloaded mouse hearts[J].Am J Physiol Heart Circ Physiol,2014,307:H1307-1316.
[30]	JAVADOV S,PURDHAM D M,ZEIDAN A,et al.NHE-1 inhibition improves cardiac mitochondrial function through regulation of mitochondrial biogenesis during postinfarction remodeling[J].Am J Physiol Heart Circ Physiol,2006,291:H1722-1730.
[31]	DONG J,ZHAO J,ZHANG M,et al.beta3-adrenoceptor impairs mitochondrial biogenesis and energy metabolism during rapid atrial pacing-induced atrial fibrillation[J].J Cardiovasc Pharmacol Ther,2016,21:114-126.