Autophagy, or "self-eating," is a conserved cellular process that degrades protein and organelle components, playing essential roles in survival, development, and homeostasis. Initially discovered over 40 years ago, autophagy has been linked to various physiological and pathological processes, including cancer, neurodegeneration, and microbial infection. The term "autophagy" was coined by de Duve in 1963 to describe the presence of single- or double-membrane vesicles containing cytoplasmic and organelle components. Early studies identified the involvement of autophagy in nutrient and energy homeostasis during starvation and the clearance of damaged proteins and organelles. The molecular control of autophagy was revolutionized in the late 1990s with the identification of the target of rapamycin (TOR) kinase, which integrates nutrient, metabolic, and hormonal signals to regulate autophagy. Subsequent studies identified key molecular components and pathways involved in autophagy, including the Atg proteins and phosphatidylinositol 3-kinase (PI3K) pathway. Autophagy has been implicated in a wide range of diseases, such as cancer, where impaired autophagy can lead to tumor development and resistance to chemotherapy. In neurodegenerative diseases, autophagy plays a crucial role in the clearance of aggregated proteins. Autophagy also influences immune responses, aging, and developmental processes. The complex regulation of autophagy and its dual role in both cell survival and death highlight the need for further research to understand its precise functions in various contexts.Autophagy, or "self-eating," is a conserved cellular process that degrades protein and organelle components, playing essential roles in survival, development, and homeostasis. Initially discovered over 40 years ago, autophagy has been linked to various physiological and pathological processes, including cancer, neurodegeneration, and microbial infection. The term "autophagy" was coined by de Duve in 1963 to describe the presence of single- or double-membrane vesicles containing cytoplasmic and organelle components. Early studies identified the involvement of autophagy in nutrient and energy homeostasis during starvation and the clearance of damaged proteins and organelles. The molecular control of autophagy was revolutionized in the late 1990s with the identification of the target of rapamycin (TOR) kinase, which integrates nutrient, metabolic, and hormonal signals to regulate autophagy. Subsequent studies identified key molecular components and pathways involved in autophagy, including the Atg proteins and phosphatidylinositol 3-kinase (PI3K) pathway. Autophagy has been implicated in a wide range of diseases, such as cancer, where impaired autophagy can lead to tumor development and resistance to chemotherapy. In neurodegenerative diseases, autophagy plays a crucial role in the clearance of aggregated proteins. Autophagy also influences immune responses, aging, and developmental processes. The complex regulation of autophagy and its dual role in both cell survival and death highlight the need for further research to understand its precise functions in various contexts.