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<p>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.</p>

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O-GlcNAc as ammonia-induced glycosylation during the development of hyperammonemia

  • 期刊论文

  • 发表日期：

    2025年11月4日

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  • Hongmei Li,
  • Yuhui Zhao,
  • Zhaoyang Sun,
  • Zeyu Zhao,
  • Siyu Hou,
  • Tao Lin,
  • Tangfei Chen,
  • Jianglong Wu,
  • Qinghong Chen,
  • Chen Zhang,
  • Zheng Li,
  • Jiajun Yang

摘要

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.