DeMorrow Sharon
Department of Medical Physiology, Texas A&M College of Medicine, Temple, TX 76504, USA.
Central Texas Veterans Healthcare System, Temple, TX 76504, USA.
J Clin Exp Hepatol. 2019 Jan-Feb;9(1):117-124. doi: 10.1016/j.jceh.2018.04.011. Epub 2018 May 4.
Hepatic encephalopathy describes the array of neurological complications that arise due to liver insufficiency and/or portal-systemic shunt. The pathogenesis of hepatic encephalopathy shares a longstanding association with hyperammonemia and inflammation. Recently, aberrant bile acid signaling has been implicated in the development of key features of hepatic encephalopathy due to acute liver failure including neuronal dysfunction, neuroinflammation and blood-brain barrier permeability. This review summarizes the findings of recent studies demonstrating a role for bile acids in hepatic encephalopathy and speculates on the possible downstream consequences of bile acid signaling.
肝性脑病描述了因肝功能不全和/或门体分流而出现的一系列神经并发症。肝性脑病的发病机制长期以来与高氨血症和炎症相关。最近,异常的胆汁酸信号传导与急性肝衰竭所致肝性脑病的关键特征的发展有关,包括神经元功能障碍、神经炎症和血脑屏障通透性。本综述总结了近期研究结果,这些研究表明胆汁酸在肝性脑病中发挥作用,并推测了胆汁酸信号传导可能产生的下游后果。