【】Myocardial hypertrophy is characterized by the heart"s deleterious response to various stressors, leading to an increase in the size of cardiomyocytes and subsequent cardiac dysfunction. Autophagy is a catabolic degradation process necessary for maintaining cellular homeostasis, and has become an important mechanism for the development of myocardial hypertrophy in recent years. This review draws on insights from recent molecular, cellular, and pharmacological studies to comprehensively explore the dual role of autophagy compounds in myocardial hypertrophy. We investigated the contribution of autophagy flux in cardiomyocytes under physiological and pathological conditions, highlighting the complex interactions between autophagy and cardiomyocyte growth, survival, and function. In addition, we discuss the potential of modulating autophagic activity through drugs as a treatment for myocardial hypertrophy and heart failure. A critical examination of established models and the exploration of new autophagy regulators bring us closer to elucidating the complex mechanisms that control myocardial hypertrophy and facilitate the development of targeted therapies. Ongoing research in this area is expected to elucidate the definitive role of autophagy regulators, providing insights into their therapeutic potential and implications for clinical interventions in myocardial hypertrophy and related pathologies.