Abstract
Inflammatory bowel disease (IBD), which include Crohn’s disease (CD) and ulcerative colitis (UC), exhibits a complex multifactorial pathogenesis involving genetic susceptibility, imbalance of gut microbiota, mucosal immune disorder and environmental factors. Recent studies reported associations between ubiquitination and deubiquitination and the occurrence and development of inflammatory bowel disease. Ubiquitination modification, one of the most important types of post-translational modifications, is a multi-step enzymatic process involved in the regulation of various physiological processes of cells, including cell cycle progression, cell differentiation, apoptosis, and innate and adaptive immune responses. Alterations in ubiquitination and deubiquitination can lead to various diseases, including IBD. Here, we review the role of E3 ubiquitin ligases and deubiquitinases (DUBs) and their mediated ubiquitination and deubiquitination modifications in the pathogenesis of IBD. We highlight the importance of this type of posttranslational modification in the development of inflammation, and provide guidance for the future development of targeted therapeutics in IBD.
Highlights
1.1 General Introduction of IBDInflammatory bowel disease (IBD) constitutes a group of chronic non-specific intestinal inflammatory disease which includes Crohn’s disease (CD) and ulcerative colitis (UC)
These results suggested that the deubiquitinase activity of CYLD in intestinal epithelial cells (IECs) plays an important inhibitory role in the process of colitisassociated carcinogenesis
Much effort has been made to elucidate the molecular mechanisms underlying the pathogenesis of IBD
Summary
Inflammatory bowel disease (IBD) constitutes a group of chronic non-specific intestinal inflammatory disease which includes Crohn’s disease (CD) and ulcerative colitis (UC). In the past 10 years, more than 200 gene loci associated with IBD have been identified in genomewide association studies (GWAS) [8, 10, 11] These susceptibility gene loci are related to the barrier function, epithelial repair, microbial defence, innate immune regulation, autophagy, adaptive immune regulation, endoplasmic reticulum stress, and others [12], and are functions known to play important roles in the pathogenesis of IBD. The general consensus is that the gut microbiota is the target of inappropriate immune response in genetically susceptible individuals, which is considered to be one of the main factors associated with the pathogenesis of IBD [16]. Environmental exposures due to urbanization, such as westernization of diets, increased use of antibiotics, smoking, microbial exposure and pollution can promote intestinal inflammation in genetically susceptible individuals by affecting the intestinal microbiome, leading to the development of IBD [19, 20]
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