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<p>Inflammatory bowel diseases (IBD), including Crohn’s disease and ulcerative colitis, are complex multifactorial disorders whose pathogenesis is driven by the interplay of genetic, epigenetic, immunological, and environmental factors. Genome-wide association studies have identified more than 240 risk loci mainly affecting immune regulation, epithelial barrier function, and autophagy. In addition to polygenic risk profiles, rare monogenic variants play a&#xa0;crucial role, particularly in early onset or pediatric cases, as they may entail specific therapeutic consequences. Epigenetic mechanisms such as DNA methylation, histone modifications, and microRNAs (miRNAs) mediate the interaction between environmental factors and the genome, contributing to disease initiation. Alterations in DNA methylation and dysregulation of specific miRNAs (e.g., miR-21, miR-146a, miR-155) are associated with inflammatory activity and therapeutic response. The miR-124 inducer obefazimod represents the first targeted epigenetic treatment approach in IBD. In the future, integrated genetic and epigenetic biomarkers may form the basis for personalized prevention and therapeutic strategies. Ultimately, clinical translation of these molecular insights, through molecular inflammation boards as interfaces between research and patient care, will be essential to implement precision medicine in IBD.</p>

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Genetik und Epigenetik der chronisch-entzündlichen Darmerkrankungen

  • 期刊论文

  • 发表日期：

    2026年3月26日

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  • Florian Tran,
  • Finn Hinrichsen,
  • Philip Rosenstiel,
  • Andre Franke

摘要

Inflammatory bowel diseases (IBD), including Crohn’s disease and ulcerative colitis, are complex multifactorial disorders whose pathogenesis is driven by the interplay of genetic, epigenetic, immunological, and environmental factors. Genome-wide association studies have identified more than 240 risk loci mainly affecting immune regulation, epithelial barrier function, and autophagy. In addition to polygenic risk profiles, rare monogenic variants play a crucial role, particularly in early onset or pediatric cases, as they may entail specific therapeutic consequences. Epigenetic mechanisms such as DNA methylation, histone modifications, and microRNAs (miRNAs) mediate the interaction between environmental factors and the genome, contributing to disease initiation. Alterations in DNA methylation and dysregulation of specific miRNAs (e.g., miR-21, miR-146a, miR-155) are associated with inflammatory activity and therapeutic response. The miR-124 inducer obefazimod represents the first targeted epigenetic treatment approach in IBD. In the future, integrated genetic and epigenetic biomarkers may form the basis for personalized prevention and therapeutic strategies. Ultimately, clinical translation of these molecular insights, through molecular inflammation boards as interfaces between research and patient care, will be essential to implement precision medicine in IBD.