Bile acids and their receptors: Potential therapeutic targets in inflammatory bowel disease

被引:5
|
作者
Long, Xiong-Quan [1 ]
Liu, Ming-Zhu [1 ]
Liu, Zi-Hao [1 ]
Xia, Lv-Zhou [1 ]
Lu, Shi-Peng [1 ]
Xu, Xiao-Ping [1 ]
Wu, Ming-Hao [1 ,2 ]
机构
[1] Hunan Normal Univ, Hunan Prov Peoples Hosp, Dept Gastroenterol, Affiliated Hosp 1, Changsha 410005, Hunan Province, Peoples R China
[2] Hunan Normal Univ, Hunan Prov Peoples Hosp, Dept Gastroenterol, Affiliated Hosp 1, 61 Jiefang West Rd, Changsha 410005, Hunan Province, Peoples R China
基金
中国国家自然科学基金;
关键词
Bile acids; Inflammatory bowel disease; Intestinal immunology; Bile acid receptors; Bile acid metabolism; Gut microbiota; FECAL MICROBIOTA TRANSPLANTATION; VITAMIN-D-RECEPTOR; ULCERATIVE-COLITIS; URSODEOXYCHOLIC ACID; NUCLEAR RECEPTOR; X RECEPTOR; INTESTINAL INFLAMMATION; DEOXYCHOLIC-ACID; CROHNS-DISEASE; SEQUESTRANTS;
D O I
10.3748/wjg.v29.i27.4252
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Chronic and recurrent inflammatory disorders of the gastrointestinal tract caused by a complex interplay between genetics and intestinal dysbiosis are called inflammatory bowel disease. As a result of the interaction between the liver and the gut microbiota, bile acids are an atypical class of steroids produced in mammals and traditionally known for their function in food absorption. With the development of genomics and metabolomics, more and more data suggest that the pathophysiological mechanisms of inflammatory bowel disease are regulated by bile acids and their receptors. Bile acids operate as signalling molecules by activating a variety of bile acid receptors that impact intestinal flora, epithelial barrier function, and intestinal immunology. Inflammatory bowel disease can be treated in new ways by using these potential molecules. This paper mainly discusses the increasing function of bile acids and their receptors in inflammatory bowel disease and their prospective therapeutic applications. In addition, we explore bile acid metabolism and the interaction of bile acids and the gut microbiota.
引用
收藏
页码:4252 / 4270
页数:19
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