Role of ETS2 gene in inflammatory bowel disease: A narrative review

The ETS2 gene, a member of the ETS (E26 transformation-specific) family of transcription factors, plays a critical role in the regulation of immune responses, epithelial barrier integrity, and fibrosis, all of which are central to the pathogenesis of inflammatory bowel disease (IBD). This review explores the molecular characteristics of ETS2, its involvement in immune dysregulation, and its contribution to IBD-associated complications, including fibrosis and colorectal cancer. ETS2 regulates key inflammatory pathways such as NF-κB and JAK-STAT, influencing cytokine production and immune cell polarization. Additionally, it affects epithelial barrier function by modulating tight junction proteins, thereby impacting intestinal permeability. Dysregulation of ETS2 expression can exacerbate intestinal inflammation, promote fibrosis, and increase the risk of colorectal cancer in IBD patients. Genetic variants of ETS2 have been associated with disease susceptibility, suggesting its potential as a biomarker for disease progression. Furthermore, targeting ETS2 may provide novel therapeutic strategies for IBD by modulating inflammatory pathways, restoring epithelial integrity, and preventing fibrosis and cancer. Understanding the role of ETS2 in IBD pathogenesis could lead to more personalized treatment approaches and improved clinical outcomes. This review highlights the potential of ETS2 as a therapeutic target and underscores the need for further research to elucidate its precise molecular mechanisms in IBD.