During evolution, eukaryotic organisms develop diverse strategies to effectively handle stressors in a manner often specifically selected to address certain intracellular threats within the cells. While several biotic and abiotic stressors are well reported, there is increasing interest in environmental pollutants due to their nexus with health, environmental sustainability, and food security, of which plants are the primary subject. In plants, the survival mechanisms employed during stress responses vary to promote survival, and in view of the sequestration pathway, previous studies have elucidated the complex transcriptional regulatory networks involved in plants' heavy metal stress response. The translational regulation and mechanisms underlying organellar remodeling and homeostasis remain elusive in plants. Here we hypothesize that autophagy, an evolutionarily conserved process that mediates the spatiotemporal degradation of superfluous cellular constituents through autophagosome formation and subsequent fusion with the vacuole, may play a crucial role in maintaining plant cellular homeostasis under heavy metal stress in a highly regulated manner. Exploring an autophagy-deficient mutant in a mixed heavy metal coupled system, we investigated the germination, growth, and survival rates of Arabidopsis thaliana. The chlorophyll profile revealed a concentration-dependent relationship with the survival rate. All ATG8 family genes were upregulated by heavy metal stress and an increased formation of YFP-ATG8e-labeled autophagic structures and the autophagic flux was observed. ATG8 lipidation analysis indicated that heavy metal stresses impact plant autophagic activity in a time-dependent manner. So far, our results indicated that heavy metals are stress inducers of autophagy that can be potentially engineered for sustainable agriculture.