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Gut microbiota modulate intestinal inflammation by endoplasmic reticulum stress-autophagy-cell death signaling axis

文献类型： 外文期刊

作者： He, Feiyang 1 ; Zheng, Yi 1 ; Elsabagh, Mabrouk 4 ; Fan, Kewei 3 ; Zha, Xia 1 ; Zhang, Bei 1 ; Wang, Mengzhi 1 ; Zhang, Hao 1 ;

作者机构： 1.Yangzhou Univ, Coll Anim Sci & Technol, Lab Metab Manipulat Herbivorous Anim Nutr, Yangzhou 225009, Peoples R China

2.Yangzhou Univ, Joint Int Res Lab Agr & Agriprod Safety, Minist Educ China, Yangzhou 225009, Peoples R China

3.Longyan Univ, Key Lab Fujian Univ Prevent Vet Med & Biotechnol, Longyan 364012, Peoples R China

4.Nigde Omermer Halisdemir Univ, Fac Agr Sci & Technol, Dept Anim Prod & Technol, TR-51240 Nigde, Turkiye

5.Xinjiang Acad Agr Reclamat Sci, State Key Lab Sheep Genet Improvement & Hlth Prod, Shihezi 832000, Peoples R China

关键词： Autophagy; Cell death; Endoplasmic reticulum stress; Gut microbes; Intestinal inflammation

期刊名称：JOURNAL OF ANIMAL SCIENCE AND BIOTECHNOLOGY （ 影响因子：6.5； 五年影响因子：7.2 ）

ISSN： 1674-9782

年卷期： 2025 年 16 卷 1 期

页码：

收录情况： SCI

摘要： The intestinal tract, a complex organ responsible for nutrient absorption and digestion, relies heavily on a balanced gut microbiome to maintain its integrity. Disruptions to this delicate microbial ecosystem can lead to intestinal inflammation, a hallmark of inflammatory bowel disease (IBD). While the role of the gut microbiome in IBD is increasingly recognized, the underlying mechanisms, particularly those involving endoplasmic reticulum (ER) stress, autophagy, and cell death, remain incompletely understood. ER stress, a cellular response to various stressors, can trigger inflammation and cell death. Autophagy, a cellular degradation process, can either alleviate or exacerbate ER stress-induced inflammation, depending on the specific context. The gut microbiome can influence both ER stress and autophagy pathways, further complicating the interplay between these processes. This review delves into the intricate relationship between ER stress, autophagy, and the gut microbiome in the context of intestinal inflammation. By exploring the molecular mechanisms underlying these interactions, we aim to provide a comprehensive theoretical framework for developing novel therapeutic strategies for IBD. A deeper understanding of the ER stress-autophagy axis, the gut microbial-ER stress axis, and the gut microbial-autophagy axis may pave the way for targeted interventions to restore intestinal health and mitigate the impact of IBD.

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