Hepatic encephalopathy (HE) may occur in patients with liver failure. The most critical pathophysiologic mechanism of HE is cerebral edema following systemic hyperammonemia. The dysfunctional liver cannot eliminate circulatory ammonia, so its plasma and brain levels rise sharply. Astrocytes, the only cells that are responsible for ammonia detoxification in the brain, are dynamic cells with unique phenotypic properties that enable them to respond to small changes in their environment. Any pathological changes in astrocytes may cause neurological disturbances such as HE. Astrocyte swelling is the leading cause of cerebral edema, which may cause brain herniation and death by increasing intracranial pressure. Various factors may have a role in astrocyte swelling. However, the exact molecular mechanism of astrocyte swelling is not fully understood. This article discusses the possible mechanisms of astrocyte swelling which related to hyperammonia, including the possible roles of molecules like glutamine, lactate, aquaporin-4 water channel, 18 KDa translocator protein, glial fibrillary acidic protein, alanine, glutathione, toll-like receptor 4, epidermal growth factor receptor, glutamate, and manganese, as well as inflammation, oxidative stress, mitochondrial permeability transition, ATP depletion, and astrocyte senescence. All these agents and factors may be targeted in therapeutic approaches to HE.

中文翻译：

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肝性脑病中星形胶质细胞肿胀：细胞毒性水肿的分子视角。

肝衰竭患者可能会发生肝性脑病（HE）。HE的最关键的病理生理机制是系统性高氨血症后的脑水肿。功能失调的肝脏无法消除循环氨，因此血浆和大脑水平急剧上升。星形胶质细胞是负责大脑中氨解毒的唯一细胞，是具有独特表型特性的动态细胞，可使其对环境的微小变化做出反应。星形胶质细胞的任何病理变化都可能引起神经系统疾病，例如HE。星形胶质细胞肿胀是脑水肿的主要原因，脑水肿可能通过增加颅内压导致脑疝和死亡。多种因素可能在星形胶质细胞肿胀中起作用。但是，星形胶质细胞肿胀的确切分子机制尚不完全清楚。本文讨论了与高氨血症相关的星形胶质细胞肿胀的可能机制，包括谷氨酰胺，乳酸盐，aquaporin-4水通道，18 KDa转运蛋白，神经胶质纤维酸性蛋白，丙氨酸，谷胱甘肽，toll​​样受体4等分子的可能作用。 ，表皮生长因子受体，谷氨酸和锰，以及炎症，氧化应激，线粒体通透性转变，ATP耗竭和星形胶质细胞衰老。所有这些试剂和因素都可能成为HE治疗方法的靶标。表皮生长因子受体，谷氨酸和锰，以及炎症，氧化应激，线粒体通透性转变，ATP耗竭和星形胶质细胞衰老。所有这些因素和因素都可能成为HE治疗方法的靶标。表皮生长因子受体，谷氨酸和锰，以及炎症，氧化应激，线粒体通透性转变，ATP耗竭和星形胶质细胞衰老。所有这些因素和因素都可能成为HE治疗方法的靶标。