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肝性脑病的病理生理基础:氨与炎症的核心作用

The pathophysiologic basis of hepatic encephalopathy: central role for ammonia and inflammation.

作者信息

Shawcross D, Jalan R

机构信息

Institute of Hepatology, University College London, 69-75 Chenies Mews, London, WC1E 6HX, United Kingdom.

出版信息

Cell Mol Life Sci. 2005 Oct;62(19-20):2295-304. doi: 10.1007/s00018-005-5089-0.

DOI:10.1007/s00018-005-5089-0
PMID:16158192
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11139067/
Abstract

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome associated with both acute and chronic liver dysfunction. It defines prognosis in acute liver injury in which patients can succumb with brain oedema and intracranial hypertension. In cirrhosis, it occurs insidiously, causing a range of neuropsychiatric disturbances. For over a century, we have known that ammonia is important in its pathogenesis and astrocytes are the cells that have been most commonly found to be affected neuropathologically. In this review we centre on the story of the 'sick astrocyte', focusing on the molecular pathogenesis of HE and the important role that inflammation has on its modulation. We describe new developments in this area with respect to potential targets for future therapies.

摘要

肝性脑病(HE)是一种与急慢性肝功能障碍相关的神经精神综合征。它决定了急性肝损伤患者的预后,这些患者可能会因脑水肿和颅内高压而死亡。在肝硬化中,它隐匿发生,导致一系列神经精神障碍。一个多世纪以来,我们已经知道氨在其发病机制中很重要,星形胶质细胞是在神经病理学上最常被发现受到影响的细胞。在这篇综述中,我们聚焦于“患病星形胶质细胞”的故事,重点关注肝性脑病的分子发病机制以及炎症在其调节中的重要作用。我们描述了该领域在未来治疗潜在靶点方面的新进展。