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Myocardial energy metabolism pathways comprise the network of biochemical processes responsible for generating ATP in the heart. The adult myocardium primarily uses fatty acid oxidation for energy (60–90% of ATP), with glucose, lactate, ketone bodies, and amino acids as additional substrates[1][2][3][4][5]. The regulation and flexibility of these pathways are essential for cardiac function and adaptation to changing physiological or pathological conditions. Dysregulation or impairment of cardiac metabolism is a central feature in various forms of heart disease, such as heart failure and ischemia[1][2][4][5]. Therapeutic strategies targeting myocardial metabolism, including agents directing substrate preference, mitochondrial function, or energy efficiency, are under investigation for treating cardiovascular diseases[2][5]. The processes involved are not a discrete target, but rather coordinated systems regulated by multiple enzymes (e.g., CPT1 for fatty acid entry, PDK4 for glucose oxidation), transcription factors (e.g., PPARs, PGC-1α), and signaling pathways[1][2][4]. In summary, "myocardial energy metabolism pathways" is not a molecular target but rather a functional and regulatory framework encompassing numerous enzymatic steps and transporters in cardiac energy metabolism.
Modulation of substrate utilization (e.g., shifting from fatty acid to glucose oxidation), mitochondrial function enhancement, reduction of oxidative stress.
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