Gastric cancer is a highly prevalent malignant tumor worldwide that typically progresses through a precancerous lesion stage, including chronic atrophic gastritis, intestinal metaplasia, and dysplasia. Mouse models of gastric precancerous lesions have recently played a significant role in studies examining the mechanisms of gastric carcinogenesis, its pathological features, and drug interventions. This article systematically summarizes the research progress in animal models of gastric precancerous lesions, including spontaneous, chemically induced, transgenic,infection, diet-induced, cell transplantation, and radiation-induced models. By simulating the histological features (e. g. , glandular atrophy, intestinal metaplasia) and molecular biological characteristics (e. g. , activation of nuclear factor-κB(NF-κB) and Wnt / β-catenin signaling pathways, role of inflammatory mediators) of gastric precancerous lesions, these models provide a multidimensional experimental platform for studying the pathogenesis of gastric cancer. Furthermore, model studies have revealed close associations between gastric precancerous lesions and various pathogenic factors, such as Helicobacter pylori infection, gene mutations, and chemical carcinogens. Existing models,however, still have certain limitations in terms of replicating the complexity, genetic heterogeneity, and tumor microenvironment of human gastric precancerous lesions. This review provides a comprehensive reference for the selection and application of gastric precancerous lesion models, providing important theoretical support for basic research and clinical translation in gastric cancer.