Autophagy is a cellular process that maintains homeostasis by degrading and recycling cellular components. It involves the formation of double-membrane vesicles called autophagosomes, which deliver cytoplasmic structures to lysosomes or vacuoles for degradation. Recent research has revealed that autophagy plays a broader role beyond degradation, including regulating metabolism, membrane transport, and immune responses. Three main types of autophagy—macroautophagy, microautophagy, and chaperone-mediated autophagy—have been identified, with macroautophagy being the focus of this review. Selective autophagy allows the targeted degradation of specific structures such as mitochondria, peroxisomes, and pathogens. This process is facilitated by autophagy receptors that recognize and bind to the cargo, enabling its sequestration into autophagosomes. The study of the yeast Cvt pathway has provided insights into selective autophagy in eukaryotic cells. Autophagy receptors often contain ubiquitin-binding domains and LIR motifs, which are crucial for cargo recognition. Post-translational modifications of Atg proteins, such as phosphorylation, ubiquitination, and acetylation, play a key role in regulating autophagy. These modifications influence the formation and function of autophagosomes, as well as the integration of autophagy with other cellular processes. For example, phosphorylation of Atg13 by yeast protein kinase A prevents its association with the phagophore assembly site, while phosphorylation of ULK1 by AMPK promotes autophagy. Autophagy is also involved in various physiological processes, including adaptation to starvation, cell differentiation, and immune responses. It contributes to the regulation of metabolism by providing metabolites for energy production and the synthesis of new macromolecules. In cancer, autophagy helps cancer cells survive under metabolic stress by reducing oxidative stress and maintaining genomic stability. However, autophagy can also inhibit tumor growth by promoting cell death. Autophagy has non-autophagic roles in cellular processes such as secretion, membrane transport, and immune responses. For example, autophagy-based unconventional secretion is involved in the release of pro-inflammatory cytokines. Autophagy also plays a role in the regulation of mitochondrial homeostasis and cell death. Additionally, autophagy is involved in the clearance of damaged organelles and the maintenance of tissue microenvironment metabolism. Despite significant advances in understanding autophagy, many aspects remain unclear, including the regulation of basal autophagy and the functional roles of Atg proteins in non-autophagic processes. Future research aims to elucidate the mechanisms underlying autophagy and its broader implications in health and disease.Autophagy is a cellular process that maintains homeostasis by degrading and recycling cellular components. It involves the formation of double-membrane vesicles called autophagosomes, which deliver cytoplasmic structures to lysosomes or vacuoles for degradation. Recent research has revealed that autophagy plays a broader role beyond degradation, including regulating metabolism, membrane transport, and immune responses. Three main types of autophagy—macroautophagy, microautophagy, and chaperone-mediated autophagy—have been identified, with macroautophagy being the focus of this review. Selective autophagy allows the targeted degradation of specific structures such as mitochondria, peroxisomes, and pathogens. This process is facilitated by autophagy receptors that recognize and bind to the cargo, enabling its sequestration into autophagosomes. The study of the yeast Cvt pathway has provided insights into selective autophagy in eukaryotic cells. Autophagy receptors often contain ubiquitin-binding domains and LIR motifs, which are crucial for cargo recognition. Post-translational modifications of Atg proteins, such as phosphorylation, ubiquitination, and acetylation, play a key role in regulating autophagy. These modifications influence the formation and function of autophagosomes, as well as the integration of autophagy with other cellular processes. For example, phosphorylation of Atg13 by yeast protein kinase A prevents its association with the phagophore assembly site, while phosphorylation of ULK1 by AMPK promotes autophagy. Autophagy is also involved in various physiological processes, including adaptation to starvation, cell differentiation, and immune responses. It contributes to the regulation of metabolism by providing metabolites for energy production and the synthesis of new macromolecules. In cancer, autophagy helps cancer cells survive under metabolic stress by reducing oxidative stress and maintaining genomic stability. However, autophagy can also inhibit tumor growth by promoting cell death. Autophagy has non-autophagic roles in cellular processes such as secretion, membrane transport, and immune responses. For example, autophagy-based unconventional secretion is involved in the release of pro-inflammatory cytokines. Autophagy also plays a role in the regulation of mitochondrial homeostasis and cell death. Additionally, autophagy is involved in the clearance of damaged organelles and the maintenance of tissue microenvironment metabolism. Despite significant advances in understanding autophagy, many aspects remain unclear, including the regulation of basal autophagy and the functional roles of Atg proteins in non-autophagic processes. Future research aims to elucidate the mechanisms underlying autophagy and its broader implications in health and disease.