The latest progress of treatment and reconstruction of energy metabolism in heart failure

doi:10.3969/j.issn.1674-490X.2015.04.011

Abstract

Abstract: Recently the reconstruction of energy metabolism has become a focus in researching the mechanism of heart failure. Reconstruction of energy metabolism is a series of complicated biochemical reactions including the transformation of energy substrates’ utilization, the abnormity of the mitochondria’s structure and function ,and changes of high-energy phosphates’ metabolism. During the further study of the complex reactions, we have found a new target and new direction for the treatment of heart failure.

Key words: heart failure；reconstruction of energy metabolism, targeted therapy

LI Li，GUO Xintong， CUI Yan，REN Yali，MA Ning，LI Xinbao，NIU Pei. The latest progress of treatment and reconstruction of energy metabolism in heart failure[J]. Medical Reserch and Education, 2015, 32(4): 44-49.

References

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Creatine kinase-mediated improvement of function in failing mouse hearts provides causal evidence the failing heart is energy starved[J]. J Clin Invest, 2012, 122(1): 291-302. [16] KARBOWSKA J, KOCHAN Z, SMOLE N / SKI R T. Peroxisome prolifeator-activated receptor alpha is downregulated in the failing human heart[J]. Cell Mol Biol Lett, 2003, 8(1): 49-53. [17] 林立. 果糖激酶和脂联素对心力衰竭心脏能量代谢的影响[J]. 心血管病学进展, 2010, 31(4) : 599-602. [18] WANG Q, DONTHI RV, WANG J, et al. Cardiac phosphatase deficient6-phosphofruto-2-kinase/fructose-2, 6-bisphosphatase increases glycolysis, hypertrophy, and myocyte resistance to hypoxia[J]. Am J Physiol, 2008, 294(6): H2889-H2897. [19] GUZUN R, TIMOHHINA N, TEPP K, et al. Systems bioenergetics of creatine kinase networks: physiological roles of creatine and phosphocreatine in regulation of cardiac cell function[J]. Amino Acids, 2011, 40(5): 1333-1348． [20] 姜鹏, 王建春, 钱桂生. 过氧化物酶增殖体激活受体与炎症及免疫反应[J]. 生命的化学, 2005, 25(3): 232-235. [21] CHINETTI G, FRUCHART J C, STAELS B. Peroxisome proliferator-activated receptors(PPARs): nuclear receptors at the crossroads between lipid metabolism and inflammation[J]. Inflamm Res, 2000, 49(10): 497-505. [22] 吴强, 杨永曜, 李隆贵, 等. 过氧化物酶体增殖物激活型受体α和γ配体对左心室压力超负荷大鼠心肌胶原重塑的影响[J]. 临床心血管病杂志, 2007, 23(2): 128-131. [23] 李俊明, 马业新, 程芳洲, 等. 大蒜素对鼠缺血再灌注心肌过氧化物酶体增殖物激活受体α表达的影响[J]. 心血管康复医学杂志, 2005, 14(4): 325-327. [24] 高瑞芳. PPARα与CaN在运动大鼠心肌微损伤与心室重塑发生中的作用[D]. 北京: 北京体育大学, 2008. [25] COLUCCI W S, KOLIAS T J, ADAMS K F, et al. Metoprolol reverses left ventricular remodeling in patients with asymptomatic systolic dysfunction[J]. Circulation, 2007, 116(1): 49-56． [26] GO A S, YANG J, GURWITZ J H, et al. Comparative effectiveness of beta-adrenergic antagonists ( atenolol, metoprolol tartrate, carvedilol) on the risk of rehospitalization in adults with heart failure[J]. Am J Cardiol, 2007, 100(4): 690-696． [27] BRISTOW M. Etomxir: a new approch to treatment of chronic heart failiure[J]. Lancet, 2000, 356(9242): 1621-1622. [28] 葛锦峰, 郑世营, 马海涛, 等. 曲美他嗪对慢性心力衰竭家兔心肌能量代谢的影响及其保护作用[J]. 苏州大学学报: 医学版, 2009, 29(6): 1089-1092. [29] 马丕勇, 李佳彧, 杨萍. 曲美他嗪对缺血性心力衰竭大鼠心脏功能与氧自由基代谢的影响[J]. 中国实验诊断学, 2011, 15(4): 614-616． [30] 沈一同. 心肌能量调节剂——曲美他嗪在心力衰竭中的应用[J]. 现代诊断与治疗, 2011, 22(1): 32-34． [31] JACOBSHAGEN C, BELARDINELLI L, HASENFUSS G, et al. Ranolazine for the treatment of heart failure with preserved ejection fraction: background, aims, and design of the RALI-DHF study[J]. Clin Cardiol, 2011, 34(7): 426-432. [32] RASTOGI S, SHAROV V G, MISHRA S, et al. Ranolazine combined with enalapril or metoprolol prevents progressive LV dysfunction and remodeling in dogs with moderate heart failure [J]. Am J Physiol Heart Cire Physiol, 2008, 295(5): H2149-H2155.