Research Division, Central Texas Veterans Health Care System, Temple, TX, USA; Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, TX, USA.
Research Division, Central Texas Veterans Health Care System, Temple, TX, USA; Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, TX, USA; Department of Internal Medicine, Dell Medical School, The University of Texas at Austin, Austin, TX, USA.
Anal Biochem. 2022 Apr 15;643:114436. doi: 10.1016/j.ab.2021.114436. Epub 2021 Oct 29.
Hepatic encephalopathy describes an array of neurological complications that arise due to liver insufficiency. The pathogenesis of hepatic encephalopathy shares a longstanding association with hyperammonemia and inflammation, and recently, aberrant bile acid signaling has been implicated in the development of key features of hepatic encephalopathy. These key features include neuronal dysfunction, neuroinflammation and blood-brain barrier permeability. This review summarizes the findings of recent studies demonstrating a role for bile acids in the pathogenesis of hepatic encephalopathy via one of three main bile acid receptors and speculates on the possible downstream consequences of aberrant bile acid signaling.
肝性脑病描述了一系列由于肝功能不全而引起的神经并发症。肝性脑病的发病机制与血氨升高和炎症长期相关,最近,异常的胆汁酸信号转导被认为与肝性脑病的关键特征的发展有关。这些关键特征包括神经元功能障碍、神经炎症和血脑屏障通透性。这篇综述总结了最近的研究结果,这些研究通过三种主要的胆汁酸受体之一,证明了胆汁酸在肝性脑病发病机制中的作用,并推测了异常胆汁酸信号转导的可能下游后果。