Autophagy is a cellular process that degrades damaged or unnecessary components through the formation of autophagosomes, which fuse with lysosomes for breakdown. It is induced by various stresses, including nutrient deprivation, growth factor deprivation, ER stress, and pathogen infection. Defective autophagy contributes to diseases such as cancer, neurodegeneration, and infectious diseases. The autophagy machinery involves key genes, such as Atg proteins, and signaling pathways that regulate autophagy in response to stress. Recent advances highlight the molecular mechanisms that regulate autophagy at multiple levels, including transcriptional activation and post-translational modifications. The Atg proteins function in various steps of autophagy, including induction, cargo recognition, and vesicle formation. The Cvt pathway is a selective autophagy pathway that delivers proteins to the vacuole. Selective autophagy targets specific cargos, such as damaged organelles or ubiquitinated proteins. Autophagosome formation involves the assembly of membranes at the phagophore assembly site (PAS). The class III PtdIns3K complex, including Vps34, Vps15, Atg14, and Atg6/Vps30, is essential for autophagy. The Atg12-Atg5-Atg16 complex and Atg8-PE conjugation systems regulate membrane elongation and expansion of autophagosomes. The Atg9 protein is essential for autophagosome formation and transport. Autophagosome-lysosome fusion and degradation of the inner vesicle are mediated by lysosomal hydrolases. Non-Atg components, such as the secretory and endocytic pathways, also contribute to autophagy. Signaling pathways, including TOR, Ras/PKA, and insulin/IGF pathways, regulate autophagy in response to nutrient and growth factor availability. ER stress, hypoxia, and oxidative stress induce autophagy through various mechanisms, including the activation of UPR pathways and the release of Ca²⁺. Pathogen infection triggers autophagy to eliminate invading pathogens. Transcriptional regulation of autophagy involves factors such as FoxO3, which induces the expression of autophagy genes. Epigenetic modifications, such as histone acetylation, also regulate autophagy. Autophagy is essential for maintaining cellular homeostasis and survival under stress conditions.Autophagy is a cellular process that degrades damaged or unnecessary components through the formation of autophagosomes, which fuse with lysosomes for breakdown. It is induced by various stresses, including nutrient deprivation, growth factor deprivation, ER stress, and pathogen infection. Defective autophagy contributes to diseases such as cancer, neurodegeneration, and infectious diseases. The autophagy machinery involves key genes, such as Atg proteins, and signaling pathways that regulate autophagy in response to stress. Recent advances highlight the molecular mechanisms that regulate autophagy at multiple levels, including transcriptional activation and post-translational modifications. The Atg proteins function in various steps of autophagy, including induction, cargo recognition, and vesicle formation. The Cvt pathway is a selective autophagy pathway that delivers proteins to the vacuole. Selective autophagy targets specific cargos, such as damaged organelles or ubiquitinated proteins. Autophagosome formation involves the assembly of membranes at the phagophore assembly site (PAS). The class III PtdIns3K complex, including Vps34, Vps15, Atg14, and Atg6/Vps30, is essential for autophagy. The Atg12-Atg5-Atg16 complex and Atg8-PE conjugation systems regulate membrane elongation and expansion of autophagosomes. The Atg9 protein is essential for autophagosome formation and transport. Autophagosome-lysosome fusion and degradation of the inner vesicle are mediated by lysosomal hydrolases. Non-Atg components, such as the secretory and endocytic pathways, also contribute to autophagy. Signaling pathways, including TOR, Ras/PKA, and insulin/IGF pathways, regulate autophagy in response to nutrient and growth factor availability. ER stress, hypoxia, and oxidative stress induce autophagy through various mechanisms, including the activation of UPR pathways and the release of Ca²⁺. Pathogen infection triggers autophagy to eliminate invading pathogens. Transcriptional regulation of autophagy involves factors such as FoxO3, which induces the expression of autophagy genes. Epigenetic modifications, such as histone acetylation, also regulate autophagy. Autophagy is essential for maintaining cellular homeostasis and survival under stress conditions.