Myocardial hypertrophy is characterized by the deleterious response of the heart to various stressors, leading to an increase in cardiomyocyte size and subsequent cardiac dysfunction. Autophagy, as a catabolic degradation process necessary for maintaining cellular homeostasis, has recently become an important mechanism in relation to the development of myocardial hypertrophy. Drawing on insights from recent molecular, cellular, and pharmacological studies, this review comprehensively explores the dual roles of autophagy compounds in myocardial hypertrophy. We investigated the contribution of autophagy flux in cardiomyocytes under physiological and pathological conditions, highlighting the complex interactions among autophagy and cardiomyocyte growth, survival, and function. In addition, we discuss the potential of modulating autophagic activity using drugs for the treatment of myocardial hypertrophy and heart failure. A critical examination of established models and the exploration of new autophagy regulators will further our understanding of the complex mechanisms that control myocardial hypertrophy and facilitate the development of targeted therapies. Ongoing research is expected to elucidate the definitive role of autophagy regulators, providing insights into their therapeutic potential and implications for clinical interventions in patients with myocardial hypertrophy and related pathologies.