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ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R
Volume 42 Issue 5
May  2026
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Article Contents

Multiorgan crosstalk in the pathogenesis of hepatic encephalopathy

DOI: 10.12449/JCH260533
Research funding:

2022 General Project of Philosophy and Social Science Research in Jiangsu Universities (2022SJYB1865);

2023 General Project of Education Research Topic of Nanjing Medical University (2023ZC104);

The Second Phase of ‘Scientific Research Talent Training Plan’ at Kangda College of Nanjing Medical University (KD2022KYRC012)

More Information
  • Corresponding author: SONG Dong, songdong@njmu.edu.cn (ORCID: 0009-0002-2432-2779)
  • Received Date: 2025-10-14
  • Accepted Date: 2025-10-27
  • Published Date: 2026-05-25
  • Hepatic encephalopathy is a common and serious complication of end-stage liver diseases such as liver cirrhosis, and it is basically a neuropsychiatric syndrome resulting from metabolic disorders caused by severe acute or chronic liver dysfunction or portosystemic shunt. In clinical practice, the onset of hepatic encephalopathy does not completely correlate linearly with the level of blood ammonia and is often triggered by extrahepatic factors, suggesting the presence of complex multiorgan crosstalk in the pathogenesis of hepatic encephalopathy. Based on the four main pathogeneses of ammonia toxicity, inflammation, neurotransmitter imbalance, and oxidative/nitrosative stress, this article systematically elaborates on the mechanism of multiorgan crosstalk in hepatic encephalopathy and discusses the emerging risk factors such as sarcopenia and diabetes mellitus, in order to provide a novel theoretical framework for deepening the understanding of the pathophysiological mechanisms of hepatic encephalopathy and formulating clinical diagnosis and treatment strategies in the future.

     

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