Fig. 2

Metabolic alterations in the aged heart. a Under an aging condition, ATP production is reduced. b Although the aged heart takes up more lipid, myocardial fatty acid oxidation is reduced concomitant with an accumulation of lipids. In parallel, glycolysis is uncoupled from glucose oxidation, leading to an accumulation of advanced glycation end-products (AGE), as a by-product of glycolysis, which, together with accumulated myocardial intralipids, promotes inflammation and alters intracellular redox condition, as well as the modification of protein, lipid, and DNA. As a result, mitochondrial dysfunction and the formation of reactive oxygen species, such as \({\mathrm{O}}_{2 }^{ \cdot -}\), exceeds the antioxidative capacity, resulting in endothelial dysfunction, cell injury, and cardiac dysfunction. ATP adenosine triphosphate, CD36 cluster of differentiation 36, SOD superoxide dismutase, TCA tricarboxylic acid