Institute of Biochemistry and Molecular Biology I, Medical Faculty, Heinrich Heine University Duesseldorf, 40225 Duesseldorf, Germany.
Division of Cardiology, Pulmonology and Vascular Medicine, Medical Faculty, Heinrich Heine University Duesseldorf, 40225 Duesseldorf, Germany.
Biomolecules. 2023 Feb 19;13(2):396. doi: 10.3390/biom13020396.
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome derived from metabolic disorders due to various liver failures. Clinically, HE is characterized by hyperammonemia, EEG abnormalities, and different degrees of disturbance in sensory, motor, and cognitive functions. The molecular mechanism of HE has not been fully elucidated, although it is generally accepted that HE occurs under the influence of miscellaneous factors, especially the synergistic effect of toxin accumulation and severe metabolism disturbance. This review summarizes the recently discovered cellular mechanisms involved in the pathogenesis of HE. Among the existing hypotheses, ammonia poisoning and the subsequent oxidative/nitrosative stress remain the mainstream theories, and reducing blood ammonia is thus the main strategy for the treatment of HE. Other pathological mechanisms mainly include manganese toxicity, autophagy inhibition, mitochondrial damage, inflammation, and senescence, proposing new avenues for future therapeutic interventions.
肝性脑病（HE）是一种由各种肝衰竭引起的代谢紊乱导致的神经精神综合征。临床上，HE 的特征是血氨升高、脑电图异常以及感觉、运动和认知功能的不同程度障碍。HE 的分子机制尚未完全阐明，尽管人们普遍认为 HE 是在多种因素的影响下发生的，特别是毒素积累和严重代谢紊乱的协同作用。本综述总结了最近发现的与 HE 发病机制相关的细胞机制。在现有的假说中，氨中毒及其随后的氧化/硝化应激仍然是主流理论，因此降低血氨是治疗 HE 的主要策略。其他病理机制主要包括锰毒性、自噬抑制、线粒体损伤、炎症和衰老，为未来的治疗干预提供了新的途径。
