Gastric intestinal metaplasia (GIM) is a precancerous lesion characterized by the replacement of normal gastric mucosa with intestinal-type epithelium. As a critical intermediate stage in the Correa cascade, which is the established model of stepwise progression toward intestinal-type gastric cancer (GC), GIM represents a key window for clinical intervention. A comprehensive understanding of the molecular and histopathological features underlying GIM pathogenesis is therefore essential for improving patient stratification and outcomes. This review synthesizes current evidence regarding the histological classification and global epidemiology of GIM, then dissect the multifactorial risk factors and underlying pathogenic mechanisms, including the intricate interplay of Helicobacter pylori infection, host susceptibility, cellular reprogramming (with an emphasis on pyloric metaplasia and SPEM), microbial dysbiosis, and immune microenvironment alterations. Furthermore, we summarize validated and emerging biomarkers associated with GIM and their predictive value for malignant transformation. By navigating these complexities, this review aims to provide a foundational framework for advancing precision medicine approaches to intercept the metaplasia-carcinoma sequence and ultimately reduce the global burden of gastric cancer.
He et al. (2026) studied this question.
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