Psoriasis, a chronic inflammatory skin disease prevalent worldwide, is primarily characterized by epidermal hyperplasia, abnormal keratinization, and immune cell infiltration, exerting a significant negative impact on patients’ quality of life and mental well-being. The onset of this disease is closely associated with genetic susceptibility, immune dysregulation, and environmental factors. Although significant progress has been made in the research on the pathogenesis of psoriasis, the existing treatment methods still have problems such as limited efficacy and obvious side-effects. Therefore, it is extremely urgent to conduct an in-depth analysis of its pathological network and develop novel intervention strategies. Against this backdrop, the imiquimod-induced psoriasis animal model has become a crucial tool for studying psoriasis due to its high reproducibility and excellent pathological simulation. This review systematically summarizes the core mechanism of action of the imiquimod-induced psoriasis model, elaborately expounds on the molecular basis of its action through pathways such as the cascade reaction of the core immune-inflammatory axis, the multi-regulatory network of downstream synergistic mechanisms, and the interaction between host and environmental factors. Research based on this model has successfully verified the therapeutic effects of various targeted therapies and natural products on psoriasis, fully demonstrating its important application value in therapeutic intervention research. In addition, the limitations of the imiquimod-induced psoriasis model are discussed, and the future research directions are prospected, aiming to provide references for in-depth research and treatment of psoriasis.