Abstract
Cardiac lipotoxicity results from the deleterious effects of excess lipid deposition in cardiomyocytes. Lipotoxic cardiomyopathy involves cardiac lipid overload leading to changes in myocardial structure and function. Cardiac dysfunction has been associated with cardiac lipotoxicity through abnormal lipid metabolism. Lipid accumulation, especially saturated free fatty acids (SFFAs), in cardiac cells can cause cardiomyocyte distress and subsequent myocardial contractile dysfunction. Reducing the excess FAs supply or promoting FA storage is beneficial for cardiac function, especially under a lipotoxic condition. The protective effects of several compounds against lipotoxicity progression in the heart have been investigated. A variety of mechanisms has been suggested to prevent or treat cardiac lipotoxicity, including improvement of calcium homeostasis, lipid metabolism, and mitochondrial dysfunction. Known targets and signaling pathways involving a select group of chemicals that interfere with cardiac lipotoxicity pathogenesis are reviewed.
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