Figure 5.

The contribution of CD36 to the pathogenesis of diabetic cardiomyopathy (DCM). The central event in the CD36-dependent mechanism of DCM pathogenesis is a persistent increase of CD36 expression in the plasma membrane, associated with the influx of fatty acids (FAs) into cardiomyocytes and lipid deposition. Some of the effects are an alteration of cardiomyocyte energy metabolism to the utility of FAs, and a decrease of glucose oxidation, which promotes ineffective energy production. The other is oxidative stress, caused by accumulated lipids and FA oxidation, stimulating cardiomyocyte death, hypertrophy, and fibrosis. They are followed by heart remodeling, deficient contractility, and ultimately heart failure.