Autophagy is a highly conserved intracellular degradation process essential for maintaining cellular homeostasis in eukaryotic organisms. It facilitates the removal and recycling of misfolded proteins, damaged organelles, and invading pathogens, especially under conditions of cellular stress such as nutrient deprivation, hypoxia, oxidative stress, and infection. Autophagy is classified into three major types: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). Macroautophagy, the most studied form, involves the formation of double-membrane autophagosomes that sequester cytoplasmic components and deliver them to lysosomes for degradation. Microautophagy occurs via lysosomal membrane invagination, while CMA selectively targets soluble cytosolic proteins bearing a KFERQ-like motif for direct translocation into the lysosome through LAMP2A receptors. The process is tightly regulated by nutrient-sensing signaling pathways. The Target of Rapamycin Complex 1 (TORC1) plays a central role, suppressing autophagy in nutrient-rich conditions and activating it during starvation or rapamycin treatment. TORC1 exerts its effects through modulation of the Atg1 kinase complex in yeast and its mammalian homolog ULK1, which initiates autophagosome formation. Additional regulators include the insulin/PI3K/Akt pathway, Ras/PKA signaling, and phosphatases such as the Tap42–Sit4/PP2A complex. These pathways converge to finely tune autophagic activity in response to metabolic cues. Autophagy also intersects with the immune system, participating in the clearance of intracellular pathogens and enhancing antigen presentation, thus contributing to both innate and adaptive immunity. Dysregulation of autophagy is implicated in a range of diseases, including cancer, neurodegenerative disorders, metabolic syndromes, and inflammatory conditions. While generally protective, excessive or insufficient autophagic activity can be detrimental, highlighting the need for precise control of this complex cellular process. Understanding the molecular mechanisms and physiological roles of autophagy opens avenues for targeted therapeutic interventions in numerous human diseases.

Autophagy, TORC1 signaling, Cellular homeostasis, Macroautophagy, Lysosomal degradation