Li Yue, Law Helen Ka Wai
Department of Health Technology and Informatics, Faculty of Health and Social Science, The Hong Kong Polytechnic University, Hunghom, Hong Kong SAR, China.
Front Pharmacol. 2022 Nov 14;13:1070184. doi: 10.3389/fphar.2022.1070184. eCollection 2022.
Inflammatory bowel disease (IBD) is a typical immune-mediated chronic inflammatory disorder. Following the industrialization and changes in lifestyle, the incidence of IBD in the world is rising, which makes health concerns and heavy burdens all over the world. However, the pathogenesis of IBD remains unclear, and the current understanding of the pathogenesis involves dysregulation of mucosal immunity, gut microbiome dysbiosis, and gut barrier defect based on genetic susceptibility and environmental triggers. In recent years, autophagy has emerged as a key mechanism in IBD development and progression because Genome-Wide Association Study revealed the complex interactions of autophagy in IBD, especially immunopathogenesis. Besides, autophagy markers are also suggested to be potential biomarkers and target treatment in IBD. This review summarizes the autophagy-related genes regulating immune response in IBD. Furthermore, we explore the evolving evidence that autophagy interacts with intestinal epithelial and immune cells to contribute to the inflammatory changes in IBD. Finally, we discuss how novel discovery could further advance our understanding of the role of autophagy and inform novel therapeutic strategies in IBD.
炎症性肠病（IBD）是一种典型的免疫介导的慢性炎症性疾病。随着工业化和生活方式的改变，全球IBD的发病率正在上升，这引起了全世界对健康的关注并带来了沉重负担。然而，IBD的发病机制仍不清楚，目前对发病机制的理解涉及基于遗传易感性和环境触发因素的黏膜免疫失调、肠道微生物群失调和肠道屏障缺陷。近年来，自噬已成为IBD发生和发展的关键机制，因为全基因组关联研究揭示了自噬在IBD中的复杂相互作用，尤其是免疫发病机制。此外，自噬标志物也被认为是IBD的潜在生物标志物和靶向治疗靶点。本综述总结了IBD中调节免疫反应的自噬相关基因。此外，我们探讨了不断发展的证据，即自噬与肠道上皮细胞和免疫细胞相互作用，导致IBD中的炎症变化。最后，我们讨论了新的发现如何能进一步推进我们对自噬作用的理解，并为IBD的新治疗策略提供依据。
