Inflammatory Bowel Disease (IBD) is an umbrella term for chronic conditions (e.g. Ulcerative colitis and Crohn's disease) that cause chronic inflammation in the gastrointestinal tract. Recent studies have shown that microRNA-21 plays an important role in promoting inflammatory responses by suppressing the anti-inflammatory genes. This paper presents a fifth-order adaptive self-modeling network model that shows the role of epigenetic changes in the progression of IBD under elevated miR-21 activity and evaluates a potential epigenetic therapeutic strategy targeting this mechanism. The model employs multilevel hierarchical adaptivity, where each adaptation level supervises the behavior and structural configuration of the level below it. Using this model, a simulation is constructed. The first simulation demonstrates how miR21 overexpression contributes to IBD. In the second scenario, the model demonstrates an epigenetic therapy to show the effect of antagomir-21, which inhibits miR-21. The simulation of this hypothetical therapy shows the potential to reduce inflammation and restore immune balance in IBD patients.

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Analysis of the Epigenetics Leading to Inflammatory Bowel Disease Using an Adaptive Self-modeling Network

  • Deniz Erdogan,
  • Zerrin Işik,
  • Jan Treur

摘要

Inflammatory Bowel Disease (IBD) is an umbrella term for chronic conditions (e.g. Ulcerative colitis and Crohn's disease) that cause chronic inflammation in the gastrointestinal tract. Recent studies have shown that microRNA-21 plays an important role in promoting inflammatory responses by suppressing the anti-inflammatory genes. This paper presents a fifth-order adaptive self-modeling network model that shows the role of epigenetic changes in the progression of IBD under elevated miR-21 activity and evaluates a potential epigenetic therapeutic strategy targeting this mechanism. The model employs multilevel hierarchical adaptivity, where each adaptation level supervises the behavior and structural configuration of the level below it. Using this model, a simulation is constructed. The first simulation demonstrates how miR21 overexpression contributes to IBD. In the second scenario, the model demonstrates an epigenetic therapy to show the effect of antagomir-21, which inhibits miR-21. The simulation of this hypothetical therapy shows the potential to reduce inflammation and restore immune balance in IBD patients.