Open AccessGenetic and epigenetic regulation of intestinal fibrosis
Author(s) -
Li Chao,
Kuemmerle John F
Publication year - 2016
Publication title -
ueg journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.667
H-Index - 35
eISSN - 2050-6414
pISSN - 2050-6406
DOI - 10.1177/2050640616659023
Subject(s) - disease , epigenetics , epigenome , medicine , crohn's disease , microbiome , inflammatory bowel disease , fibrosis , genetic architecture , immunology , bioinformatics , genetics , gene , biology , phenotype , pathology , dna methylation , gene expression
Crohn’s disease affects those individuals with polygenic risk factors. The identified risk loci indicate that the genetic architecture of Crohn’s disease involves both innate and adaptive immunity and the response to the intestinal environment including the microbiome. Genetic risk alone, however, predicts only 25% of disease, indicating that other factors, including the intestinal environment, can shape the epigenome and also confer heritable risk to patients. Patients with Crohn’s disease can have purely inflammatory disease, penetrating disease or fibrostenosis. Analysis of the genetic risk combined with epigenetic marks of Crohn’s disease and other disease associated with organ fibrosis reveals common events are affecting the genes and pathways key to development of fibrosis. This review will focus on what is known about the mechanisms by which genetic and epigenetic risk factors determine development of fibrosis in Crohn’s disease and contrast that with other fibrotic conditions.