In summary, our study demonstrated that A-MG relieves DCM pathology by blocking the uptake of FAs via CD36, lowering systemic hyperglycemia and lipid accumulation in cardiac tissue, preventing excessive β-oxidation of FAs and ensuing ROS production, increasing the antioxidant capacity of cardiomyocytes, and inhibiting cardiomyocyte apoptosis. The gene discussed is CD36; the disease is familial dilated cardiomyopathy.