Background and aim: The ATP-binding cassette subfamily B member 1 (ABCB1) gene, also known as MDR1, plays a crucial role in drug transport and cellular detoxification. Dysregulation of ABCB1 expression due to epigenetic modifications, such as promoter methylation, has been implicated in various inflammatory diseases, including ulcerative colitis (UC). Altered ABCB1 gene expression may affect gut barrier integrity and inflammatory response, making ABCB1 promoter methylation a potential biomarker for UC progression and severity. Methods: This study is a review study by searching scientific databases such as Scopus, PubMed, and Embase from 2016 to 2024 by using the keywords ABCB1, Ulcerative Colitis, Biomarker, Therapy., 65 articles related to inclusion criteria were extracted and then analyzed. Results: Results show that UC patients exhibit significantly higher levels of ABCB1 promoter methylation compared to controls, resulting in reduced ABCB1 expression in colonic epithelial cells. This downregulation is associated with increased intestinal permeability and inflammation, key features of UC pathology. Furthermore, elevated ABCB1 promoter methylation was correlated with disease severity, suggesting its potential as a prognostic marker. Treatment interventions, including certain anti-inflammatory drugs, were found to partially reverse methylation changes, thereby restoring ABCB1 expression. Conclusion: The findings support ABCB1 promoter methylation as a contributing factor in UC pathogenesis. Hyper-methylation leads to decreased ABCB1 expression, which compromises gut barrier function and exacerbates inflammation. Targeting epigenetic modifications to restore ABCB1 expression could offer a novel therapeutic approach for UC. Further research is needed to validate these findings in larger cohorts and explore therapeutic agents that can modulate methylation status. ABCB1 promoter methylation represents a promising biomarker and therapeutic target for managing ulcerative colitis.
