| 1 | Implication of miRNAs for inflammatory bowel disease treatment:Systematic review显示文摘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 diseaseassociated 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. | Wei-Xu Chen Li-Hua Ren Rui-Hua Shi | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，2： | 31 |
| 2 | 在煽动性的肠疾病的 Fibrogenesis 和纤维变性: 一样的硬币的好、坏的方面?显示文摘 Fibrogenesis in inflammatory bowel diseases is a complex phenomenon aimed at mucosal repair. However, it may provoke intestinal fibrosis with the development of strictures which require surgery. Therefore, fibrogenesis may be considered as a 'two-faced' process when related to chronic intestinal inflammation. Many types of cells may be converted into the fibrogenic phenotype at different levels of the intestinal wall. A complex interaction of cytokines, adhesion molecules and growth factors is involved in the process. We report an overview of recent advances in molecular mechanisms of stricturizing Crohn’s disease(CD) including the potential role of trasforming growth factor beta, protein kinase C and Ras, Raf and ERK proteins. Fibrotic growth factors such as vascular endothelial growth factor and platelet-derived growth factor, as well as the Endothelial-to-Mesenchymal Transition induced by transforming growth factor-β, are considered. Finally, our experience, focused on tumor necrosis factor α(the main cytokine of inflammatory bowel diseases) and the link between syndecan 1(a heparan sulphate adhesion molecule) and basic fibroblast growth factor(a strong stimulator of collagen synthesis) is described. We hypothesize a possible molecular pattern for mucosal healing as well as how its deregulation could be involved in fibrotic complications of CD. A final clinical point is the importance of performing an accurate evaluation of the presence of fibrotic strictures before starting anti-tumor necrosis α treatment, which could worsen the lesions. | Mariabeatrice Principi Floriana Giorgio Giuseppe Losurdo Viviana Neve Antonella Contaldo Alfredo Di Leo Enzo Ierardi | 2013 | World Journal of Gastrointestinal Pathophysiology2013，4，4： | 2 |
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