熊去氧胆酸
牛磺去氧胆酸
肝硬化
胆汁酸
胆汁淤积
医学
硼胆酸
脂肪肝
肝病
胃肠病学
内科学
疾病
生物
生物化学
细胞凋亡
受体
未折叠蛋白反应
兴奋剂
作者
Wenkang Gao,Zhonglin Li,Huikuan Chu,Hang Yuan,Lilin Hu,Lin Yao,Li Zhang,Weijun Wang,Rong Lin,Ling Yang
标识
DOI:10.1007/978-981-19-2615-0_6
摘要
Bile acids (BAs) not only play critical roles in liver-gut immune homeostasis but also participate in regulating lipid, glucose, and energy metabolism. BAs transporter defect or signaling pathways abnormal activation are linked to cholestasis, inflammation, fibrosis, carcinogenesis, and metabolic disorders. BAs and related signaling pathways have become attractive therapeutic targets for inflammation, fibrosis, and metabolic diseases, including type 2 diabetes mellitus and non-alcoholic fatty liver disease (NAFLD). Hydrophilic BAs, including ursodeoxycholic acid (UDCA), tauroursodeoxycholic (TUDCA), and 24-norursodeoxycholic (nor-UDCA), have hepatoprotective properties and are widely used in cholestatic liver diseases. Here, we provide an overview of the mechanism and recent clinical application of UDCA in hepatobiliary diseases, as well as BAs cross-talk with the gut microbiota in health and diseases. Targeting bile-acid signaling for liver cirrhosis is a promising and effective strategy. Evidences from clinical trials suggest that UDCA treatment has beneficial effects on cirrhosis.
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