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During heart failure, mitochondrial oxidative capacity is reduced by increased reactive oxygen species (ROS), dysregulated mitochondrial Ca 2+ homeostasis, impaired mitochondrial dynamics, mitochondrial autophagy and other adverse factors, leading to a reduced capacity and efficiency of fatty acid and glucose oxidation ( Many studies support the concept that ketones are alternative metabolic substrates for failing hearts

3(5): 34560 Pearson DJ, Tubbs PK, Chase JF

As a limitation, the study eliminated other databases like Google Scholar and Scopus, which would have had an impact on the quantity of papers returned, and we only used the Web of Science database

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