Abstract Autophagy is a lysosomal-dependent mechanism of cellular degradation characterized by the presence of double-membraned vesicles called autophagosomes. Increasing lines of evidence suggest that both non-selective autophagy and cargo-specific forms of autophagy, such as the mitochondria-specific form of autophagy, termed mitophagy, are activated in the heart in response to stress. However, their activation is often transient and insufficient during the chronic phase of cardiac conditions, including both pressure and volume overload, heart failure with preserved ejection fraction, obesity and diabetic cardiomyopathy, and ageing cardiomyopathy. Indeed, interventions to restore the levels of autophagy and mitophagy often alleviate cardiac dysfunction in animal models of heart failure. It is, therefore, important to understand the molecular mechanisms that inhibit or activate autophagy and mitophagy during the chronic phase of heart failure. Under some conditions, autophagy can become dysregulated in the heart and induce cellular dysfunction and death. For example, lysosomal function is attenuated through multiple mechanisms. Autosis, a specific form of cell de
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