Autophagy is a highly conserved process in eukaryotes that involves the sequestration of cytoplasm, including excess or aberrant organelles, into double-membrane vesicles, which are then delivered to the lysosome/vacuole for degradation and recycling. This process plays a crucial role in various biological events, including adaptation to environmental changes, cellular remodeling, and determining lifespan. Autophagy is also involved in preventing certain diseases but may contribute to some pathologies. Recent studies have identified many components required for this complex process. Autophagy-related genes were first identified in yeast, but homologs are found in all eukaryotes. Analyses in various model systems have advanced understanding of the molecular basis of autophagy. This review summarizes current knowledge on the machinery and molecular mechanisms of autophagy. Autophagy is evolutionarily conserved from yeast to mammals and has important roles in various cellular functions. In yeast, nutrient starvation induces autophagy, allowing unneeded proteins to be degraded and amino acids to be recycled. In higher eukaryotes, autophagy is induced in response to nutrient depletion. Autophagy is involved in physiological processes such as lifespan extension and cellular development. It may play a protective role against diseases like cancer, muscular disorders, and neurodegenerative diseases. Autophagy also acts as a cellular defense mechanism against certain pathogens. However, it is also involved in type II programmed cell death and may contribute to disease pathology. Autophagy was first morphologically identified in mammalian cells in the 1960s, but the molecular mechanism was only recently elucidated. The identification of genes involved in autophagy, particularly in yeast, has been a key breakthrough. These genes, termed ATG genes, are also found in other eukaryotes. Studies in yeast have advanced understanding of autophagy, pexophagy, and the Cvt pathway. Orthologs of ATG genes have been found in higher eukaryotes, indicating that the molecular machinery of autophagy is conserved across species. Autophagy is regulated by environmental stress, with nutrient starvation inducing it. The protein kinase Tor is a negative regulator that responds to nitrogen levels. Under nutrient-rich conditions, Tor is active and autophagy is inhibited, while under nutrient-deficient conditions, Tor is inactivated and autophagy is enhanced. The Tor protein is conserved in mammals and senses environmental changes to modulate autophagy. The Atg1-Atg13 complex interacts with multiple proteins, including Vac8, Atg11, and Atg17, which are involved in autophagy. Atg17 is required for autophagy under starvation conditions but not for the Cvt pathway under nutrient-rich conditions. The Atg1-Atg13-Atg17 complex may play a role in autophagy separate fromAutophagy is a highly conserved process in eukaryotes that involves the sequestration of cytoplasm, including excess or aberrant organelles, into double-membrane vesicles, which are then delivered to the lysosome/vacuole for degradation and recycling. This process plays a crucial role in various biological events, including adaptation to environmental changes, cellular remodeling, and determining lifespan. Autophagy is also involved in preventing certain diseases but may contribute to some pathologies. Recent studies have identified many components required for this complex process. Autophagy-related genes were first identified in yeast, but homologs are found in all eukaryotes. Analyses in various model systems have advanced understanding of the molecular basis of autophagy. This review summarizes current knowledge on the machinery and molecular mechanisms of autophagy. Autophagy is evolutionarily conserved from yeast to mammals and has important roles in various cellular functions. In yeast, nutrient starvation induces autophagy, allowing unneeded proteins to be degraded and amino acids to be recycled. In higher eukaryotes, autophagy is induced in response to nutrient depletion. Autophagy is involved in physiological processes such as lifespan extension and cellular development. It may play a protective role against diseases like cancer, muscular disorders, and neurodegenerative diseases. Autophagy also acts as a cellular defense mechanism against certain pathogens. However, it is also involved in type II programmed cell death and may contribute to disease pathology. Autophagy was first morphologically identified in mammalian cells in the 1960s, but the molecular mechanism was only recently elucidated. The identification of genes involved in autophagy, particularly in yeast, has been a key breakthrough. These genes, termed ATG genes, are also found in other eukaryotes. Studies in yeast have advanced understanding of autophagy, pexophagy, and the Cvt pathway. Orthologs of ATG genes have been found in higher eukaryotes, indicating that the molecular machinery of autophagy is conserved across species. Autophagy is regulated by environmental stress, with nutrient starvation inducing it. The protein kinase Tor is a negative regulator that responds to nitrogen levels. Under nutrient-rich conditions, Tor is active and autophagy is inhibited, while under nutrient-deficient conditions, Tor is inactivated and autophagy is enhanced. The Tor protein is conserved in mammals and senses environmental changes to modulate autophagy. The Atg1-Atg13 complex interacts with multiple proteins, including Vac8, Atg11, and Atg17, which are involved in autophagy. Atg17 is required for autophagy under starvation conditions but not for the Cvt pathway under nutrient-rich conditions. The Atg1-Atg13-Atg17 complex may play a role in autophagy separate from