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Recent studies have shown that, as the cell with the highest density of mitochondria, impaired energy metabolism in cardiomyocytes is a key pathological basis of damaged myocardium, which brings about a series of significant changes in myocardial energy and substrate metabolism, leading to metabolic remodeling, where the myocardium preferentially shifts substrates from fatty acids to glucose for utilization, and involves abnormalities in oxidative phosphorylation and a decrease in high-energy phosphates, resulting in dysfunctions in myocardial function and structure (van Bilsen et al., 2004)

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