Autophagy is a cellular process that degrades damaged components, such as proteins, organelles, and pathogens, to maintain cellular homeostasis. It plays a critical role in energy balance, cellular survival, and disease prevention, including cancer, neurodegeneration, and infections. Autophagy can be non-selective or selective, with mechanisms involving the formation of autophagosomes that fuse with lysosomes for degradation. Key molecular pathways include the Atg5-Atg12 conjugation and LC3 processing, which are essential for autophagosome formation and maturation. Autophagy is regulated by various signaling pathways, including the TOR kinase, which inhibits autophagy under nutrient-rich conditions and promotes it during starvation. The Beclin-1 complex, along with class III PI3 kinases, is crucial for autophagy initiation. Autophagy also interacts with apoptosis, with some studies suggesting it can promote or inhibit cell death depending on the context. Selective autophagy, such as mitophagy and pexophagy, targets specific organelles for degradation. Defects in autophagy have been linked to various diseases, and its role in cancer remains controversial, with some evidence suggesting it may act as a tumor suppressor or promote tumorigenesis. Understanding autophagy's molecular mechanisms and regulation is essential for developing therapeutic strategies for diseases associated with autophagy dysfunction.Autophagy is a cellular process that degrades damaged components, such as proteins, organelles, and pathogens, to maintain cellular homeostasis. It plays a critical role in energy balance, cellular survival, and disease prevention, including cancer, neurodegeneration, and infections. Autophagy can be non-selective or selective, with mechanisms involving the formation of autophagosomes that fuse with lysosomes for degradation. Key molecular pathways include the Atg5-Atg12 conjugation and LC3 processing, which are essential for autophagosome formation and maturation. Autophagy is regulated by various signaling pathways, including the TOR kinase, which inhibits autophagy under nutrient-rich conditions and promotes it during starvation. The Beclin-1 complex, along with class III PI3 kinases, is crucial for autophagy initiation. Autophagy also interacts with apoptosis, with some studies suggesting it can promote or inhibit cell death depending on the context. Selective autophagy, such as mitophagy and pexophagy, targets specific organelles for degradation. Defects in autophagy have been linked to various diseases, and its role in cancer remains controversial, with some evidence suggesting it may act as a tumor suppressor or promote tumorigenesis. Understanding autophagy's molecular mechanisms and regulation is essential for developing therapeutic strategies for diseases associated with autophagy dysfunction.