Cardiomyocyte health: adapting to metabolic changes through autophagy

• Autophagy is crucial for cardiac homeostasis.
• Cardiac autophagy is decreased in obesity, metabolic syndrome, and diabetes.
• Reduced autophagy leads to myocyte damage, cell death, and contractile dysfunction.
• Treatments enhancing cardiac autophagy may prevent diabetic cardiomyopathy.

Autophagy is important in the heart for maintaining homeostasis when changes in nutrient levels occur. Autophagy is involved in the turnover of cellular components, and is rapidly upregulated during stress. Studies have found that autophagy is reduced in metabolic disorders including obesity and diabetes. This leads to accumulation of protein aggregates and dysfunctional organelles, which contributes to the pathogenesis of cardiovascular disease. Autophagy is primarily regulated by two components: the mechanistic target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK). Although mTOR integrates information about growth factors and nutrients and is a negative regulator of autophagy, AMPK is an energy sensor and activates autophagy when energy levels are low. These pathways therefore present targets for the development of autophagy-modulating therapies.