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Mitochondrial energy metabolism in heart failure: a question of balance
Janice M. Huss, Daniel P. Kelly
Janice M. Huss, Daniel P. Kelly
Published March 1, 2005
Citation Information: J Clin Invest. 2005;115(3):547-555. https://doi.org/10.1172/JCI24405.
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Review Series

Mitochondrial energy metabolism in heart failure: a question of balance

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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.

Authors

Janice M. Huss, Daniel P. Kelly

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Figure 1

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Pathways involved in cardiac energy metabolism. FA and glucose oxidation...
Pathways involved in cardiac energy metabolism. FA and glucose oxidation are the main ATP-generating pathways in the adult mammalian heart. Acetyl-CoA derived from FA and glucose oxidation is further oxidized in the TCA cycle to generate NADH and FADH2, which enter the electron transport/oxidative phosphorylation pathway and drive ATP synthesis. Genes encoding enzymes involved at multiple steps of these metabolic pathways (i.e., uptake, esterification, mitochondrial transport,and oxidation) are transcriptionally regulated by PGC-1α with its nuclear receptor partners, including PPARs and ERRs (blue text). Glucose uptake/oxidation and electron transport/oxidative phosphorylation pathways are also regulated by PGC-1α via other transcription factors, such as MEF-2 and NRF-1. Cyt c, cytochrome c.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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