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Erschienen in: Metabolic Brain Disease 4/2020

07.03.2020 | Review Article

Astrocyte swelling in hepatic encephalopathy: molecular perspective of cytotoxic edema

verfasst von: Ali Sepehrinezhad, Asadollah Zarifkar, Gholamreza Namvar, Ali Shahbazi, Roger Williams

Erschienen in: Metabolic Brain Disease | Ausgabe 4/2020

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Abstract

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.
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Metadaten
Titel
Astrocyte swelling in hepatic encephalopathy: molecular perspective of cytotoxic edema
verfasst von
Ali Sepehrinezhad
Asadollah Zarifkar
Gholamreza Namvar
Ali Shahbazi
Roger Williams
Publikationsdatum
07.03.2020
Verlag
Springer US
Erschienen in
Metabolic Brain Disease / Ausgabe 4/2020
Print ISSN: 0885-7490
Elektronische ISSN: 1573-7365
DOI
https://doi.org/10.1007/s11011-020-00549-8

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