Oxidative Stress in Inflammatory Bowel Disease: From Redox Dysregulation to Translational Targeting.

Oxidative stress has emerged as an important component of the complex pathophysiology of inflammatory bowel disease (IBD), where increasing evidence suggests an interaction between redox imbalance, immune activation, epithelial dysfunction, and chronic intestinal inflammation. This structured narrative review critically synthesizes current evidence regarding the biological basis of oxidative stress in IBD, with emphasis on cellular and molecular mechanisms, oxidative biomarkers, therapeutic modulation of redox pathways, and their translational relevance. Current evidence indicates that oxidative stress is associated with immune-cell activation, mitochondrial dysfunction, impairment of epithelial homeostasis, and dysregulation of redox-sensitive signaling pathways. Biomarkers including nitric oxide metabolites, malondialdehyde, myeloperoxidase, total antioxidant capacity, serum thiols, and antioxidant enzymes have demonstrated associations with inflammatory activity, while anti-inflammatory, antioxidant, and dietary interventions have been reported to modulate oxidative biomarkers in selected clinical studies. However, substantial methodological heterogeneity, variability in analytical techniques, and limited prospective validation currently restrict their routine clinical application. Moreover, many mechanistic pathways have been characterized predominantly in experimental models, highlighting the need to distinguish biological plausibility from evidence supporting clinical implementation. Overall, oxidative stress represents a promising area of investigation that may contribute to a better understanding of IBD biology and support future biomarker-guided and precision medicine approaches. Nevertheless, further standardized translational and longitudinal clinical studies are required before oxidative biomarkers and redox-targeted strategies can be integrated into routine patient care.