ArticleJournal of molecular histology2025
O-GlcNAc as ammonia-induced glycosylation during the development of hyperammonemia.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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12 authors.
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Abstract
Hyperammonemia is a key pathological feature of hepatic encephalopathy (HE), yet its associated protein glycosylation remains incompletely understood. Here, we used whole mouse brain tissues from a hyperammonemia mouse model and astrocytes to conduct a comprehensive analysis of glycosylation changes and the corresponding enzyme associated with ammonia. The upregulation of O-linked N-acetylglucosamine (O-GlcNAc), mediated by O-GlcNAc transferase, was identified as a response to ammonia stimulation in astrocytes through a mechanism independent of glutamine synthesis and NADPH oxidase. These findings identify O-GlcNAc as an ammonia-sensitive post-translational modification that is associated with hyperammonemia. This study provides new insights into the molecular mechanisms of HE and suggests the potential role of O-GlcNAc as a therapeutic target warranting further investigation.
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