Key result
Metabolic remodeling precedes and sustains functional and structural remodeling in the diseased heart, making it a potential target for pharmacological intervention to restore metabolic flexibility.
This paper proposes that restoring metabolic flexibility in the diseased heart could be a viable pharmacological target to improve contractile function.
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Should not yet alter heart disease management; leaves open whether restoring metabolic flexibility improves outcomes in trials.
Metabolism transfers energy from substrates to ATP. As a "metabolic omnivore," the normal heart adapts to changes in the environment by switching from one substrate to another. We propose that this flexibility is lost in the maladapted, diseased heart. Both adaptation and maladaptation are the results of metabolic signals that regulate transcription of key cardiac regulatory genes. We propose that metabolic remodeling precedes, initiates, and sustains functional and structural remodeling. The process of metabolic remodeling then becomes a target for pharmacological intervention restoring metabolic flexibility and normal contractile function of the heart.
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Taegtmeyer et al. (2004) conducted a review in Diseased heart. Pharmacological intervention targeting metabolic remodeling was evaluated. Metabolic remodeling precedes and sustains functional and structural remodeling in the diseased heart, making it a potential target for pharmacological intervention to restore metabolic flexibility.
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