[1]陈忠秀,综述,饶莉,等.线粒体能量代谢异常与病理性心肌肥大的研究进展[J].心血管病学进展,2016,(3):247-250.[doi:10.16806/j.cnki.issn.1004-3934.2016.03.008]
 CHEN Zhongxiu,RAO Li.Mitochondrial Energy Metabolism and Pathological Cardiac Hypertrophy[J].Advances in Cardiovascular Diseases,2016,(3):247-250.[doi:10.16806/j.cnki.issn.1004-3934.2016.03.008]
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线粒体能量代谢异常与病理性心肌肥大的研究进展()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2016年3期
页码:
247-250
栏目:
综述
出版日期:
2016-06-20

文章信息/Info

Title:
Mitochondrial Energy Metabolism and Pathological Cardiac Hypertrophy
作者:
陈忠秀综述饶莉审校
四川大学华西医院心内科,四川 成都 610041
Author(s):
CHEN Zhongxiu RAO Li
Department of Cardiology,West China Hospital,Sichuan University, Chengdu 610041,Sichuan,China
关键词:
线粒体 能量代谢 心肌肥大
Keywords:
Mitochondria Energy metabolism Cardiac hypertrophy
分类号:
R542.2
DOI:
10.16806/j.cnki.issn.1004-3934.2016.03.008
文献标志码:
A
摘要:
病理性心肌肥大是临床常见的适应性改变过程,伴随着能量代谢类型的转变及线粒体生物学功能的衰退,是心血管疾病发生率和病死率增高的独立危险因素。肥大心肌细胞能量代谢异常与多条信号通路异常关系密切,改善能量代谢异常有望成为逆转心肌肥大和延缓心力衰竭进程治疗的新靶点。
Abstract:
Pathological cardiac hypertrophy is a coadaptive process accompanied by metabolic profile change and mitochondrial bioenergetic decline, and is an independent predictor of higher rate of cardiovascular events and mortality. Many signaling pathways are involved in the maladaptive metabolism of hypertrophied hearts, and targeting abnormal metabolism is likely the new therapy of hypertrophic prevention and reversion.

参考文献/References:

[1] Kolwicz Jr SC, Tian R. Glucose metabolism and cardiac hypertrophy[J]. Cardiovasc Res,2011,90(2):194-201.
[2] Cramariuc D, Gerdts E, Davidsen ES, et al. Myocardial deformation in aortic valve stenosis: relation to left ventricular geometry[J]. Heart,2010,96(2):106-112.
[3] Cioffi G, Faggiano P, Vizzardi E, et al. Prognostic effect of inappropriately high left ventricular mass in asymptomatic severe aortic stenosis[J]. Heart,2011,97(4): 301-307.
[4] Mureddu GF, Cioffi G, Stefenelli C, et al. Compensatory or inappropriate left ventricular mass in different models of left ventricular pressure overload:comparison between patients with aortic stenosis and arterial hypertension[J]. J Hypertens,2009, 27(3):642-649.
[5] Doenst T, Pytel G, Schrepper A, et al. Decreased rates of substrate oxidation ex vivo predict the onset of heart failure and contractile dysfunction in rats with pressure overload[J]. Cardiovasc Res,2010,86(3):461-470.
[6] Razeghi P,Young ME,Alcorn JL,et al.Metabolic gene expression in fetal and failing human heart[J]. Circulation,2001,104(24):2923-2931.
[7] Leong HS, Grist M, Parsons H, et al. Accelerated rates of glycolysis in the hypertrophied heart:are they a methodological artifact?[J]. Am J Physiol Endocrinol Metab,2002,282(5):E1039-E1045.
[8] Nascimben L, Ingwall JS, Lorell BH, et al. Mechanisms for increased glycolysis in the hypertrophied rat heart[J]. Hypertension,2004,44(5):662-667.
[9] Tian R,Musi N,D'Agostino J, et al. Increased adenosine monophosphate-activated protein kinase activity in rat hearts with pressure-overload hypertrophy[J]. Circulation,2001,104(14):1664-1669.
[10] Allard MF,Wambolt RB,Longnus SL,et al. Hypertrophied rat hearts are less responsive to the metabolic and functional effects of insulin[J]. Am J Physiol Endocrinol Metab,2000,279(3):E487-E493.
[11] Grifn JL, Donnell JM, White LT, et al. Postnatal expression and activity of the mitochondrial 2-oxoglutarate-malate carrier in intact hearts[J]. Am J Physiol Cell Physiol,2000,279(6):1704-1709.
[12] Dai DF, Johnson SC, Villarin JJ, et al. Mitochondrial oxidative stress mediates angiotensin Ⅱ-induced cardiac hypertrophy and Galphaq overexpression-induced heart failure[J]. Circ Res,2011,108(7):837-846.
[13] Griffiths ER, Friehs I, Scherr E,et al. Electron transport chain dysfunction in neonatal pressure-overload hypertrophy precedes cardiomyocyte apoptosis independent of oxidative stress[J]. J Thorac Cardiovasc Surg,2010,139(6):1609-1617.
[14] Gong G, Liu J, Liang P, et al. Oxidative capacity in failing hearts[J]. Am J Physiol Heart Circ Physiol,2003,285(2):H541-H548.
[15] 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.
[16] 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.
[17] Barger PM,Brandt JM,Leone TC,et al.Deactivation of peroxisome proliferator-activated receptor-alpha during cardiac hypertrophic growth[J]. J Clin Invest,2000,105(12):1723-1730.
[18] Akki A,Smith K,Seymour AM. Compensated cardiac hypertrophy is characterised by a decline in palmitate oxidation[J]. Mol Cell Biochem,2008,311(1-2):215-224.
[19] Lam VH,Zhang L,Huqi A,et al. Activating PPARα prevents post-ischemic contractile dysfunction in hypertrophied neonatal hearts[J]. Circ Res,2015, 117(1):41-51.
[20] Meng RS, Pei ZH, Zhang AX, et al. AMPK activation enhances PPARa activity to inhibit cardiac hypertrophy via ERK1/2 MAPK signaling pathway[J].Arch Biochem Biophys,2011,511(1-2):1-7.
[21] 黄秋菊,黄金贤,罗佳妮,等. ERK1 /2 /PPARα/SCAD 信号途径对生理性和病理性心肌肥大的调控[J].中国病理生理杂志,2014,30(8):1427-1432.
[22] Hasumi Y, Baba M, Hasumi H, et al. Folliculin(Flcn)inactivation leads to murine cardiac hypertrophy through mTORC1 deregulation[J]. Hum Mol Genet,2014, 23(21):5706-5719.
[23] Pillai VB, Samant S, Sundaresan NR, et al. Honokiol blocks and reverses cardiac hypertrophy in mice by activating mitochondrial Sirt3[J]. Nat Commun,2015,6:6656.
[24] Yu HJ,Tigchelaar W,Koonen DPY,et al. AKIP1 expression modulates mitochondrial function in rat neonatal cardiomyocytes[J]. PLoS One,2013,8(11): e80815.
[25] Tigchelaar W, Yu HJ, de Jong AM, et al. Loss of mitochondrial exo/endonuclease EXOG affects mitochondrial respiration and induces ROS-mediated cardiomyocyte hypertrophy[J]. Am J Physiol Cell Physiol,2015,308(2):C155-C163.
[26] Domenighetti AA, Danes VR, Curl CL, et al. Targeted GLUT-4 deciency in the heart induces cardiomyocyte hypertrophy and impaired contractility linked with Ca(2+)and proton ux dysregulation[J]. J Mol Cell Cardiol,2010,48(4):663-672.
[27] Hamilton DJ,Zhang A,Li S,et al.Combination of Angiotensin Ⅱ and L-NG-Nitroarginine methyl ester exacerbates mitochondrial dysfunction and oxidative stress to cause heart failure[J]. Am J Physiol Heart Circ Physiol,2016,310(6):H667-H680.
[28] Kobara M, Furumori-Yukiya A, Kitamura M, et al. Short-term caloric restriction suppresses cardiac oxidative stress and hypertrophy caused by chronic pressure overload[J]. J Card Fail,2015,21(8):656-666.
[29] Poornima I, Brown SB, Bhashyam S, et al. Chronic glucagon-like peptide-1 infusion sustains left ventricular systolic function and prolongs survival in the spontaneously hypertensive, heart failure-prone rat[J]. Circ Heart Fail, 2008,1(3):153-160.
[30] Vitale C, Wajngaten M, Sposato B, et al. Trimetazidine improves left ventricular function and quality of life in elderly patients with coronary artery disease[J]. Eur Heart J, 2004, 25(20):1814-1821.
[31] 张晶,王洪新,宋莹,等.黄芪甲苷抑制大鼠心肌肥厚及改善心肌能量代谢的作用观察[J]. 中成药, 2012, 34( 5): 924-928.
[32] 于妍,王硕仁,聂波,等.川芎嗪、缬沙坦及曲美他嗪对乳鼠肥大心肌细胞线粒体结构和能量代谢的影响[J]. 中西医结合心脑血管病杂志, 2012, 10(3): 321-324.
[33] 王燕飞,曹雪滨,徐淑乐,等.心复康口服液对慢性压力超负荷大鼠心肌能量代谢的影响[J].第三军医大学学报,2009,31(18): 1720-1723.

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备注/Memo

备注/Memo:
基金项目:国家自然科学基金青年科学基金项目(81300169) 作者简介:陈忠秀(1988—),在读博士,主要从事心肌病的基础与临床研究。Email: czxlfb1988@163.com 通信作者:饶莉(1963—),教授,主任医师,博士生导师,博士,主要从事扩张型心肌病的基础与临床和心脏瓣膜偏心反流的定量评价研究。Email: lrlz1989@163.com
更新日期/Last Update: 2016-05-25