Hepatic encephalopathy (HE) is a well-studied, neurological syndrome caused by liver dysfunctions. Ammonia, the major toxin during HE pathogenesis, impairs many cellular processes within astrocytes. Yet, the molecular mechanisms causing HE are not fully understood. Here we will recapitulate possible underlying mechanisms with a clear focus on studies revealing a link between altered energy metabolism and HE in cellular models and in vivo. The role of the mitochondrial glutamate dehydrogenase and its role in metabolic rewiring of the TCA cycle will be discussed. We propose an updated model of ammonia-induced toxicity that may also be exploited for therapeutic strategies in the future.

中文翻译：

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高氨血症下星形胶质细胞的快速代谢和生物能量适应——肝性脑病的新视角

肝性脑病 (HE) 是一种经过充分研究的由肝功能障碍引起的神经系统综合征。氨是 HE 发病过程中的主要毒素，它会损害星形胶质细胞内的许多细胞过程。然而，引起HE的分子机制尚不完全清楚。在这里，我们将重述可能的潜在机制，并明确关注揭示细胞模型中能量代谢改变与 HE 之间联系的研究，以及体内. 将讨论线粒体谷氨酸脱氢酶的作用及其在 TCA 循环代谢重新布线中的作用。我们提出了一种氨诱导毒性的更新模型，该模型也可用于未来的治疗策略。