CD36 and cardiac hypertrophy: The decrease in FA import through CD36, leading to a metabolic shift toward increased glucose utilization, hastens the transition from compensated hypertrophy (characterized by enhanced cardiac hypertrophy and interstitial fibrosis) to heart failure,[8] while the preservation of FA oxidation prevents the metabolic shift and cardiac hypertrophy development.[14] The metabolic shift and the associated alterations in gene expression, metabolite signaling, and the utilization of glucose‐derived carbon for anabolic pathways play a crucial role in the physiological growth of the heart.