Yi Joo Mi, Kim Tae Oh
Research Institute, Dongnam Institute of Radiological & Medical Sciences (DIRAMS), Busan, Korea.
Department of Internal Medicine, Haeundae Paik Hospital, Inje University College of Medicine, Busan, Korea.
Intest Res. 2015 Apr;13(2):112-21. doi: 10.5217/ir.2015.13.2.112. Epub 2015 Apr 27.
Overwhelming evidences supports the idea that inflammatory bowel disease (IBD) is caused by a complex interplay between genetic alterations of multiple genes and an aberrant interaction with environmental factors. There is growing evidence that epigenetic factors can play a significant part in the pathogenesis of IBD. Significant effort has been invested in uncovering genetic and epigenetic factors, which may increase the risk of IBD, but progress has been slow, and few IBD-specific factors have been detected so far. It has been known for decades that DNA methylation is the most well studied epigenetic modification, and analysis of DNA methylation is leading to a new generation of cancer biomarkers. Therefore, in this review, we summarize the role of DNA methylation alteration in IBD pathogenesis, and discuss specific genes or genetic loci using recent molecular technology advances. Here, we suggest that DNA methylation should be studied in depth to understand the molecular pathways of IBD pathogenesis, and discuss epigenetic studies of IBD that may have a significant impact on the field of IBD research.
大量证据支持这样一种观点,即炎症性肠病(IBD)是由多个基因的遗传改变与环境因素的异常相互作用之间的复杂相互作用引起的。越来越多的证据表明,表观遗传因素在IBD的发病机制中可能起重要作用。人们已经投入了大量精力来揭示可能增加IBD风险的遗传和表观遗传因素,但进展缓慢,迄今为止几乎没有检测到IBD特异性因素。几十年来,人们已经知道DNA甲基化是研究最深入的表观遗传修饰,对DNA甲基化的分析正在催生新一代癌症生物标志物。因此,在本综述中,我们总结了DNA甲基化改变在IBD发病机制中的作用,并利用最近的分子技术进展讨论特定基因或基因位点。在此,我们建议应深入研究DNA甲基化以了解IBD发病机制的分子途径,并讨论可能对IBD研究领域产生重大影响的IBD表观遗传学研究。