m6A modification in inflammatory bowel disease provides new insights into clinical applications - 03/02/23
Abstract |
Inflammatory bowel disease (IBD) results from a complex interplay between genetic predisposition, environmental factors, and gut microbes. The role of N6-methyladenosine (m6A) methylation in the pathogenesis of IBD has attracted increasing attention. m6A modification not only regulates intestinal mucosal immunity and intestinal barrier function, but also affects apoptosis and autophagy in intestinal epithelial cells. Additionally, m6A modification participated in the interaction between gut microbes and the host, providing a novel direction to explore the molecular mechanisms of IBD and the theoretical basis for specific microorganism-oriented prevention and treatment measures. m6A regulators are expected to be biomarkers for predicting the prognosis of IBD patients. m6A methylation may be utilized as a novel target in the management of IBD. This review focused on the recent advances in how m6A modification causes the initiation and development of IBD, and provided new insights into optimal prevention and treatment measures for IBD.
Le texte complet de cet article est disponible en PDF.Graphical Abstract |
Highlights |
• | m6A participates in the pathogenesis of inflammatory bowel disease. |
• | m6A is involved in the host–gut microbiota crosstalk. |
• | m6A may be a predictor for the progression of inflammatory bowel disease. |
• | m6A has the potential to be a target for reducing infliximab/vedolizumab resistance and thiopurine-induced myelosuppression. |
• | Targeting m6A is expected to be a novel therapy for inflammatory bowel disease. |
Keywords : M6A modification, Inflammatory bowel disease, Intestinal immunity, Intestinal barrier, IBD therapy
Plan
Vol 159
Article 114298- mars 2023 Retour au numéro
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