TL;DRAbstract
In the failing heart, there are changes in energy substrate metabolism whose etiology and effects are poorly understood. These changes may contribute to deterioration in cardiac contractility as well as to increasing left ventricular remodeling that are the landmarks of the failing heart. Early in HF, the myocardial substrate selection is relatively normal; however, with further HF progression, there is a downregulation of fatty acid oxidation (FAO), increased glycolysis and glucose oxidation, decreased mitochondrial respiratory chain activity, and abnormal mitochondrial OXPHOS. Since the literature is abundant on the subject of acquired and inherited lipid disorders in the development of coronary artery disease and stroke (e.g., cholesterol, the apolipoproteins and HDL/LDL, we have decided to omit these subjects. In this chapter, we deal with the metabolic changes that occur in progressive HF, particularly on the mechanisms that regulate metabolic genes expression and metabolic signal
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In the failing heart, there are changes in energy substrate metabolism whose etiology and effects are poorly understood. These changes may contribute to deterioration in cardiac contractility as well as to increasing left ventricular remodeling that are the landmarks of the failing heart. Early in HF, the myocardial substrate selection is relatively normal; however, with further HF progression, there is a downregulation of fatty acid oxidation (FAO), increased glycolysis and glucose oxidation, decreased mitochondrial respiratory chain activity, and abnormal mitochondrial OXPHOS. Since the literature is abundant on the subject of acquired and inherited lipid disorders in the development of coronary artery disease and stroke (e.g., cholesterol, the apolipoproteins and HDL/LDL, we have decided to omit these subjects. In this chapter, we deal with the metabolic changes that occur in progressive HF, particularly on the mechanisms that regulate metabolic genes expression and metabolic signal
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