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- W2595771123 endingPage "1944" @default.
- W2595771123 startingPage "1944" @default.
- W2595771123 abstract "Inflammatory bowel disease (IBD) results from a complex series of interactions between susceptibility genes, the environment, and the immune system. Recently, some studies provided strong evidence that the process of autophagy affects several aspects of mucosal immune responses. Autophagy is a cellular stress response that plays key roles in physiological processes, such as innate and adaptive immunity, adaptation to starvation, degradation of aberrant proteins or organelles, antimicrobial defense, and protein secretion. Dysfunctional autophagy is recognized as a contributing factor in many chronic inflammatory diseases, including IBD. Autophagy plays multiple roles in IBD pathogenesis by altering processes that include intracellular bacterial killing, antimicrobial peptide secretion by Paneth cells, goblet cell function, proinflammatory cytokine production by macrophages, antigen presentation by dendritic cells, and the endoplasmic reticulum stress response in enterocytes. Recent studies have identified susceptibility genes involved in autophagy, such as NOD2, ATG16L1, and IRGM, and active research is ongoing all over the world. The aim of this review is a systematic appraisal of the current literature to provide a better understanding of the role of autophagy in the pathogenesis of IBD. Understanding these mechanisms will bring about new strategies for the treatment and prevention of IBD." @default.
- W2595771123 created "2017-03-23" @default.
- W2595771123 creator A5000086080 @default.
- W2595771123 creator A5002391399 @default.
- W2595771123 creator A5071238305 @default.
- W2595771123 date "2017-01-01" @default.
- W2595771123 modified "2023-10-18" @default.
- W2595771123 title "Role of autophagy in the pathogenesis of inflammatory bowel disease" @default.
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