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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Gastroenterol. Dec 21, 2026; 32(47): 122954
Published online Dec 21, 2026. doi: 10.3748/wjg.122954
Bile acid metabolic disorders and their role in hepatic encephalopathy of cirrhosis
Yu-Jie Huo, Zi-Xin Liang, Jing-Xuan Bian, Jing-Tian Zhang, Li Cha, Qi-Yue Yang, Chun-Juan Zhao, Jin-Yu Li, Dui-Ping Feng, Long Gao
Yu-Jie Huo, Qi-Yue Yang, Chun-Juan Zhao, Jin-Yu Li, Dui-Ping Feng, Long Gao, Department of Oncological and Vascular Intervention, First Hospital of Shanxi Medical University, Taiyuan 030001, Shanxi Province, China
Yu-Jie Huo, Zi-Xin Liang, Jing-Xuan Bian, Jing-Tian Zhang, Li Cha, Department of Medical Imaging, Shanxi Medical University, Taiyuan 030001, Shanxi Province, China
Co-first authors: Yu-Jie Huo and Zi-Xin Liang.
Co-corresponding authors: Long Gao and Dui-Ping Feng.
Author contributions: Huo YJ and Liang ZX contributed equally to this work, conceptualized and designed the study, conducted the investigation, visualised the data, and drafted the original manuscript as co-first authors; Bian JX, Zhang JT, Cha L, and Yang QY critically reviewed and revised the manuscript; Zhao CJ and Li JY provided critical feedback and manuscript revisions; Feng DP and Gao L supervised the study and made critical revisions as co-corresponding authors; all authors approved the final version and publication of the manuscript.
AI contribution statement: Portions of this manuscript were edited using AI tools solely for language refinement. The authors carefully reviewed and verified all AI-assisted outputs and take full responsibility for the scientific content of the manuscript.
Supported by the Shanxi Provincial Clinical Research Center for Interventional Medicine, No. 202204010501004; and the Central Government Guiding Local Science and Technology Development Funds, No. YDZJSX20231B010.
Conflict-of-interest statement: All authors declare no conflict of interest in publishing the manuscript.
Corresponding author: Long Gao, PhD, Associate Chief Physician, Department of Oncological and Vascular Intervention, First Hospital of Shanxi Medical University, No. 85 Jiefang South Road, Yingze District, Taiyuan 030001, Shanxi Province, China. gaolong@sxmu.edu.cn
Received: May 12, 2026
Revised: July 12, 2026
Accepted: July 28, 2026
Published online: December 21, 2026
Processing time: 177 Days and 16.9 Hours
Core Tip

Core Tip: Cirrhosis disrupts bile acid (BA) homeostasis, creating a vicious cycle with gut dysbiosis and barrier injury. Accumulated toxic BAs cross the blood-brain barrier and modulate neuroinflammation via farnesoid X receptor, Takeda G protein-coupled receptor 5, and Sphingosine-1-phosphate receptor 2 signaling, synergizing with hyperammonemia to drive hepatic encephalopathy. BA profiles vary by cirrhosis etiology, offering diagnostic and prognostic potential. Targeting BA pathways represents a promising therapeutic strategy for hepatic encephalopathy.

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