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Implication of miRNAs for inflammatory bowel disease treatment: systematic review

Chen WX, Ren LH, Shi RH2014World Journal of Gastrointestinal PathophysiologyReview
10.4291/wjgp.v5.i2.63PubMedFree full text
GastrointestinalImmune/Innate

Abstract

Inflammatory bowel disease (IBD) is believed to develop via a complex interaction between genetic, environmental factors and the mucosal immune system. Crohn's disease and ulcerative colitis are two major clinical forms of IBD. MicroRNAs (miRNAs) are a class of small, endogenous, noncoding RNA molecules, and evolutionary conserved in animals and plants. It controls protein production at the post-transcriptional level by targeting mRNAs for translational repression or degradation. MiRNAs are important in many biological processes, such as signal transduction, cellular proliferation, differentiation and apoptosis. Considerable attention has been paid on the key role of miRNAs in autoimmune and inflammatory disease, especially IBD. Recent studies have identified altered miRNA profiles in ulcerative colitis, Crohn's disease and inflammatory bowel disease-associated colorectal cancer. In addition, emerging data have implicated that special miRNAs which suppress functional targets play a critical role in regulating key pathogenic mechanism in IBD. MiRNAs were found involving in regulation of nuclear transcription factor kappa B pathway (e.g., miR-146a, miR-146b, miR-122, miR-132, miR-126), intestinal epithelial barrier function (e.g., miR-21, miR-150, miR-200b) and the autophagic activity (e.g., miR-30c, miR-130a, miR-106b, miR-93, miR-196). This review aims at discussing recent advances in our understanding of miRNAs in IBD pathogenesis, their role as disease biomarkers, and perspective for future investigation and clinical application.

Key Biomarkers

miR-106bmiR-122miR-126miR-130amiR-132miR-146amiR-146bmiR-150miR-196miR-200bmiR-21miR-30cmiR-93

Symptom Clusters

Autophagy dysregulationCrohn's diseaseInflammatory bowel diseaseIntestinal epithelial barrier dysfunctionNF-κB pathway dysregulationUlcerative colitis

References (1)

  • Cai W. miR-200b inhibits TGF-B1-induced epithelial-mesenchymal transition and promotes growth of intestinal epithelial cellsEducational Technology & Society · 2013

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