Abstract
Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the colonic mucosa. Environmental factors, genetics, intestinal microbiota, and the immune system are all involved in the pathophysiology of IBD. Lately, accumulating evidence has shown that abnormal epigenetic changes in DNA methylation, histone markers, and non-coding RNA expression greatly contribute to the development of the entire disease. Epigenetics regulates many functions, such as maintaining the homeostasis of the intestinal epithelium and regulating the immune system of the immune cells. In the present study, we systematically summarized the latest advances in epigenetic modification of IBD and how epigenetics reveals new mechanisms of IBD. Our present review provided new insights into the pathophysiology of IBD. Moreover, exploring the patterns of DNA methylation and histone modification through epigenetics can not only be used as biomarkers of IBD but also as a new target for therapeutic intervention in IBD patients.
Highlights
As a chronic inflammatory disease, inflammatory bowel disease (IBD) is characterized by recurrent abdominal pain and diarrhea, and its subtypes include ulcerative colitis (UC) and Crohn’s disease (CD)
To emphasize the importance of epigenetic mechanisms for Inflammatory bowel disease (IBD), we reviewed the effects of DNA methylation, histone modification, non-coding RNA, and epigenetic modification on T and B immune cells in IBD
In addition to identifying the progression of IBD by the methylation status of individual genes, other researchers have indicated that we can conduct total epigenome-wide association studies (EWAS)-related research using genome-wide related research methods to observe the correlation between disease progression and differentially methylated genes in IBD patients
Summary
Reviewed by: Antonella Fazio, University Medical Center HamburgEppendorf, Germany Celia Escudero-Hernández, University Medical Center SchleswigHolstein, Germany. Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the colonic mucosa. Environmental factors, genetics, intestinal microbiota, and the immune system are all involved in the pathophysiology of IBD. Accumulating evidence has shown that abnormal epigenetic changes in DNA methylation, histone markers, and non-coding RNA expression greatly contribute to the development of the entire disease. We systematically summarized the latest advances in epigenetic modification of IBD and how epigenetics reveals new mechanisms of IBD. Our present review provided new insights into the pathophysiology of IBD. Exploring the patterns of DNA methylation and histone modification through epigenetics can be used as biomarkers of IBD and as a new target for therapeutic intervention in IBD patients
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