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Especially under ischemiareperfusion conditions, reducing the level of acylcarnitine has a significant effect on the energy metabolism of the heart and the maturity and proliferation of cardiomyocytes because reducing the utilization of fatty acids and increasing the reliance on glucose oxidation as an energy source can promote the recovery of myocardial function at a lower rate of oxygen consumption

Its deleterious effects are primarily mediated through oxidative stress, neuroinflammatory responses, and apoptotic pathways