Oxidative Stress Mechanisms in Inflammatory Bowel Disease

Inflammatory bowel disease (IBD), encompassing Crohn’s disease and ulcerative colitis, is driven in part by a sustained imbalance between the generation of reactive oxygen species (ROS) and the capacity of local antioxidant defences. Excessive ROS production by activated epithelial cells, infiltrating neutrophils and macrophages leads to lipid peroxidation, protein oxidation and DNA damage within the intestinal mucosa. Disruption of epithelial barrier integrity ensues, facilitating translocation of luminal antigens and commensal bacteria that further amplify mucosal inflammation. At the same time, certain ROS species function as redox messengers, modulating key transcription factors such as NF-κB and Nrf2, and influencing cytokine networks, cell death pathways and wound-healing responses. Genetic variations affecting antioxidant enzymes, mitochondrial function or redox-sensitive signalling cascades predispose individuals to exaggerated oxidative injury. Epigenetic alterations and dysbiosis also interact with oxidative stress to shape disease onset and progression. A clearer understanding of precise ROS sources, redox-feedback loops and patient-specific redox signatures offers the prospect of tailored interventions that restore mucosal homeostasis, protect barrier function and reduce reliance on broad immunosuppression. This mechanistic insight underpins the global quest for robust biomarkers and mechanism-based therapies to limit the burden of IBD and improve long-term outcomes.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Oxidative Stress Mechanisms in Inflammatory Bowel Disease publication trend

The graph below shows the total number of articles in oxidative stress mechanisms in inflammatory bowel disease across all publications each year (not limited to Nature Index journals).

Technical terms

Reactive oxygen species (ROS): Highly reactive molecules derived from oxygen that can damage cellular components.
Redox signalling: Biological communication mediated by oxidation–reduction reactions that regulate cell functions.
Antioxidant enzymes: Proteins such as superoxide dismutase or catalase that neutralise ROS.
Mendelian randomisation: A genetic epidemiology method using genetic variants to infer causal relationships.
Epigenetics: Heritable changes in gene expression not involving alterations in DNA sequence.
Plant-derived nanovesicles: Nano-sized vesicles extracted from plants that carry bioactive compounds.

References

1. Personalized redox medicine in inflammatory bowel diseases: an emerging role for HIF-1α and NRF2 as therapeutic targets. Redox Biology (2023).
2. Oxidative stress gene expression, DNA methylation, and gut microbiota interaction trigger Crohn’s disease: a multi-omics Mendelian randomization study. BMC Medicine (2023).
3. Industrial-produced lemon nanovesicles ameliorate experimental colitis-associated damages in rats via the activation of anti-inflammatory and antioxidant responses and microbiota modification. Biomedicine & Pharmacotherapy (2024).