Key result
During cardiac remodeling, myocardial fuel preference switches from fatty acids to glucose, leading to metabolic changes that could serve as potential therapeutic targets in heart failure.
This review highlights the shift in myocardial energy metabolism during heart failure and identifies metabolic pathways as potential therapeutic targets.
Metabolic switch during remodeling may drive lipotoxicity and impair ATP; leaves open whether targeting substrate preference alters HF progression.
Fatty acids are the main substrates used by mitochondria to provide myocardial energy under normal conditions. During heart remodeling, however, the fuel preference switches to glucose. In the earlier stages of cardiac remodeling, changes in energy metabolism are considered crucial to protect the heart from irreversible damage. Furthermore, low fatty acid oxidation and the stimulus for glycolytic pathway lead to lipotoxicity, acidosis, and low adenosine triphosphate production. While myocardial function is directly associated with energy metabolism, the metabolic pathways could be potential targets for therapy in heart failure.
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Azevedo et al. (2012) conducted a review in Cardiac remodeling and heart failure. During cardiac remodeling, myocardial fuel preference switches from fatty acids to glucose, leading to metabolic changes that could serve as potential therapeutic targets in heart failure.
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