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本文引用的文献

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Cardiomyocyte-restricted peroxisome proliferator-activated receptor-delta deletion perturbs myocardial fatty acid oxidation and leads to cardiomyopathy.心肌细胞特异性过氧化物酶体增殖物激活受体δ缺失扰乱心肌脂肪酸氧化并导致心肌病。
Nat Med. 2004 Nov;10(11):1245-50. doi: 10.1038/nm1116. Epub 2004 Oct 10.
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Estrogen-related receptor alpha directs peroxisome proliferator-activated receptor alpha signaling in the transcriptional control of energy metabolism in cardiac and skeletal muscle.雌激素相关受体α在心脏和骨骼肌能量代谢的转录调控中指导过氧化物酶体增殖物激活受体α信号传导。
Mol Cell Biol. 2004 Oct;24(20):9079-91. doi: 10.1128/MCB.24.20.9079-9091.2004.
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NDUFS6 mutations are a novel cause of lethal neonatal mitochondrial complex I deficiency.NDUFS6突变是致死性新生儿线粒体复合体I缺乏症的一种新病因。
J Clin Invest. 2004 Sep;114(6):837-45. doi: 10.1172/JCI20683.
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Activation of cardiac Cdk9 represses PGC-1 and confers a predisposition to heart failure.心脏Cdk9的激活会抑制PGC-1，并使人易患心力衰竭。
EMBO J. 2004 Sep 1;23(17):3559-69. doi: 10.1038/sj.emboj.7600351. Epub 2004 Aug 5.
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Cardiac mitochondrial damage and biogenesis in a chronic model of type 1 diabetes.1型糖尿病慢性模型中的心脏线粒体损伤与生物发生
Am J Physiol Endocrinol Metab. 2004 Nov;287(5):E896-905. doi: 10.1152/ajpendo.00047.2004. Epub 2004 Jul 27.
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Calcineurin and calcium/calmodulin-dependent protein kinase activate distinct metabolic gene regulatory programs in cardiac muscle.钙调神经磷酸酶和钙/钙调蛋白依赖性蛋白激酶激活心肌中不同的代谢基因调控程序。
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Moderate severity heart failure does not involve a downregulation of myocardial fatty acid oxidation.中度心力衰竭并不涉及心肌脂肪酸氧化的下调。
Am J Physiol Heart Circ Physiol. 2004 Oct;287(4):H1538-43. doi: 10.1152/ajpheart.00281.2004. Epub 2004 Jun 10.
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Catalase protects cardiomyocyte function in models of type 1 and type 2 diabetes.过氧化氢酶在1型和2型糖尿病模型中可保护心肌细胞功能。
Diabetes. 2004 May;53(5):1336-43. doi: 10.2337/diabetes.53.5.1336.
9
Erralpha and Gabpa/b specify PGC-1alpha-dependent oxidative phosphorylation gene expression that is altered in diabetic muscle.Erralpha和Gabpa/b指定了在糖尿病肌肉中发生改变的依赖于PGC-1α的氧化磷酸化基因表达。
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The estrogen-related receptor alpha (ERRalpha) functions in PPARgamma coactivator 1alpha (PGC-1alpha)-induced mitochondrial biogenesis.雌激素相关受体α（ERRα）在过氧化物酶体增殖物激活受体γ共激活因子1α（PGC-1α）诱导的线粒体生物发生过程中发挥作用。
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心力衰竭中的线粒体能量代谢：平衡问题

Mitochondrial energy metabolism in heart failure: a question of balance.

作者信息

Huss Janice M, Kelly Daniel P

机构信息

Center for Cardiovascular Research, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

出版信息

J Clin Invest. 2005 Mar;115(3):547-55. doi: 10.1172/JCI24405.

DOI:10.1172/JCI24405
PMID:15765136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1052011/
Abstract

The mitochondrion serves a critical role as a platform for energy transduction, signaling, and cell death pathways relevant to common diseases of the myocardium such as heart failure. This review focuses on the molecular regulatory events and downstream effector pathways involved in mitochondrial energy metabolic derangements known to occur during the development of heart failure.

摘要

线粒体作为能量转导、信号传导以及与心肌常见疾病（如心力衰竭）相关的细胞死亡途径的平台，发挥着关键作用。本综述聚焦于心力衰竭发展过程中已知会发生的线粒体能量代谢紊乱所涉及的分子调控事件和下游效应途径。