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Energy metabolism pathways in the myocardium are an interconnected set of biochemical processes that enable the heart to generate ATP to support contractile function. Major pathways include glycolysis, glucose oxidation, fatty acid oxidation, and ketone body oxidation. Substrate selection and metabolic flux are dynamically regulated to match cardiac energy demand. Dysfunction in these pathways is associated with heart failure, cardiomyopathy, diabetes, and other cardiac diseases. While individual enzymes and transporters within these pathways (e.g., pyruvate dehydrogenase, carnitine palmitoyltransferase, glucose transporters) are valid drug targets, the collective pathway itself is not a canonical molecule, receptor, or single therapeutic target[1][3][4][5].
Drugs modulate specific enzymes or transporter activity within the myocardium, shifting substrate preference (e.g., from fatty acid to glucose oxidation) or increasing efficiency of ATP production
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