Epigenetic modification of m6A methylation: Regulatory factors, functions and mechanism in inflammatory bowel disease
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Updated: Jul 9, 2025

Chronic Salmonella Infection Induced Intestinal Fibrosis
Published on: September 22, 2019
Yanping Wang1, Chaoyue Chen1, Wei Yan2
1Department of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Abstract:
Although the exact cause of inflammatory bowel disease (IBD) is still unknown, there is a lot of evidence to support the notion that it results from a combination of environmental factors, immune system issues, gut microbial changes, and genetic susceptibility. In recent years, the role of epigenetics in the pathogenesis of IBD has drawn increasing attention. The regulation of IBD-related immunity, the preservation of the intestinal epithelial barrier, and autophagy are all significantly influenced by epigenetic factors. The most extensive epigenetic methylation modification of mammalian mRNA among them is N6-methyladenosine (m6A). It summarizes the general structure and function of the m6A regulating factors, as well as their complex effects on IBD by regulating the intestinal mucous barrier, intestine mucosal immunity, epidermal cell death, and intestinal microorganisms.This paper provides key insights for the future identification of potential new targets for the diagnosis and treatment of IBD.
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