期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
卷 1833, 期 4, 页码 840-847出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2012.08.015
关键词
Heart failure; Mitochondria; Peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha); Fatty acid oxidation (FAO)
资金
- NIH [RO1 DK045416, RO1 HL058493, RO1 HL101189]
- The Swiss National Science Foundation [PBLAP3 136880]
- Swiss National Science Foundation (SNF) [PBLAP3_136880] Funding Source: Swiss National Science Foundation (SNF)
The heart is an omnivore organ that requires constant energy production to match its functional demands. In the adult heart, adenosine-5'-triphosphate (ATP) production occurs mainly through mitochondrial fatty acid and glucose oxidation. The heart must constantly adapt its energy production in response to changes in substrate supply and work demands across diverse physiologic and pathophysiologic conditions. The cardiac myocyte maintains a high level of mitochondrial ATP production through a complex transcriptional regulatory network that is orchestrated by the members of the peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family. There is increasing evidence that during the development of cardiac hypertrophy and in the failing heart, the activity of this network, including PGC-1, is altered. This review summarizes our current understanding of the perturbations in the gene regulatory pathways that occur during the development of heart failure. An appreciation of the role this regulatory circuitry serves in the regulation of cardiac energy metabolism may unveil novel therapeutic targets aimed at the metabolic disturbances that presage heart failure. This article is part of a Special Issue entitled:Cardiomyocyte Biology: Cardiac Pathways of Differentiation, Metabolism and Contraction. (C) 2012 Elsevier B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据