Abstract: Autophagy, a highly conserved protective mechanism in eukaryotes, plays a crucial role in plant growth, development, and stress responses by degrading and recycling intracellular components. This study aims to systematically elucidate the biogenesis and physiological functions of autophagy in plants, provide a theoretical basis for further research, and explore its potential applications in improving nutrient-use efficiency and stress-resilient crop breeding. Plant autophagy comprises macroautophagy, microautophagy, and chaperone-mediated autophagy. Its biogenesis proceeds through four major stages—activation and initiation, membrane expansion, autophagosome formation, and subsequent fusion with the vacuole for degradation. These processes are precisely regulated by ATG genes and the SnRK1/TOR signaling pathways. SnRK1 regulates autophagy through both TOR-dependent and TOR-independent mechanisms, while ATG genes play key roles in each stage, including the ATG1−ATG13 complex, ATG12−ATG5−ATG16 complex, and ATG8 lipidation. Autophagy regulates root development, enhances nutrient acquisition efficiency, delays senescence, and promotes nutrient remobilization. It also enhances plant tolerance to nitrogen, phosphorus, zinc, iron, cadmium, and other micronutrient stresses, as well as abiotic stresses such as salinity, drought, high temperature, and waterlogging. Future research needs to further analyze the spatiotemporal regulatory networks of autophagy, integrate multi-omics technologies, and systematically explore its roles in nutrient transmembrane transport and its interactions with hormone signaling and nutrient metabolism. Additionally, in the context of crop breeding, emphasis should be focus on nutrient uptake efficiency, utilization, and stress resistance. This will promote "autophagy-nutrient efficiency-stress resistance" co-regulation and provide theoretical support for breeding high-efficiency, stress-resilient crops and advancing agricultural efficiency and sustainable development.