Energy metabolism in heart failure and remodelling
Top Cited Papers
Open Access
- 29 October 2008
- journal article
- review article
- Published by Oxford University Press (OUP) in Cardiovascular Research
- Vol. 81 (3) , 412-419
- https://doi.org/10.1093/cvr/cvn301
Abstract
Myocytes of the failing heart undergo impressive metabolic remodelling. The time line for changes in the pathways for ATP synthesis in compensated hypertrophy is: flux through the creatine kinase (CK) reaction falls as both creatine concentration ([Cr]) and CK activity fall; increases in [ADP] and [AMP] lead to increases in glucose uptake and utilization; fatty acid oxidation either remains the same or decreases. In uncompensated hypertrophy and in other forms of heart failure, CK flux and fatty acid oxidation are both lower; any increases in glucose uptake and utilization are not sufficient to compensate for overall decreases in the capacity for ATP supply and [ATP] falls. Metabolic remodelling is under transcriptional and post-transcriptional control. The lower metabolic reserve of the failing heart contributes to impaired contractile reserve.Keywords
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