Under salt stress, autophagy regulates ionic balance, scavenges ROS, and supports nutrient remobilization, thereby alleviating osmotic and oxidative damage. Salt stress is a major environmental challenge that significantly impacts plant growth and agricultural productivity by disrupting nutrient balance, inducing osmotic stress, and causing the accumulation of toxic ions like Na+. Autophagy, a key cellular degradation and recycling pathway, plays a critical role in enhancing plant salt tolerance by maintaining cellular homeostasis and mitigating stress-induced damage. While autophagy has traditionally been viewed as a response to nutrient starvation, recent research has highlighted its importance under various environmental stresses, particularly salt stress. Under such conditions, plants activate autophagy through distinct signaling pathways involving autophagy-related genes (ATGs), Target of Rapamycin (TOR) proteins, and reactive oxygen species (ROS). Salt stress induces the expression of ATG genes and promotes the formation of autophagosomes, which facilitate the degradation of damaged organelles, denatured proteins, and the sequestration of Na+ into vacuoles, thereby improving stress tolerance. Recent studies have also suggested that autophagy may play a direct role in salt stress signaling, linking it to the regulation of metabolic processes. This review discusses the molecular mechanisms underlying autophagy induction in plants under salt stress, including the roles of ATGs and TOR, as well as the physiological significance of autophagy in mitigating oxidative damage, maintaining ion balance, and enhancing overall salt tolerance. In addition, we discussed the metabolic changes related to autophagy in stressed plants and examined the broader implications for managing plant stress and improving crops.
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