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O-GlycNacylation Remission Retards the Progression of Non-Alcoholic Fatty Liver Disease.

Yicheng ZhouZhangwang LiMinxuan XuDeju ZhangJitao LingPeng YuYunfeng Shen
Published in: Cells (2022)
Non-alcoholic fatty liver disease (NAFLD) is a metabolic disease spectrum associated with insulin resistance (IR), from non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). O-GlcNAcylation is a posttranslational modification, regulated by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). Abnormal O-GlcNAcylation plays a key role in IR, fat deposition, inflammatory injury, fibrosis, and tumorigenesis. However, the specific mechanisms and clinical treatments of O-GlcNAcylation and NAFLD are yet to be elucidated. The modification contributes to understanding the pathogenesis and development of NAFLD, thus clarifying the protective effect of O-GlcNAcylation inhibition on liver injury. In this review, the crucial role of O-GlcNAcylation in NAFLD (from NAFL to HCC) is discussed, and the effect of therapeutics on O-GlcNAcylation and its potential mechanisms on NAFLD have been highlighted. These inferences present novel insights into the pathogenesis and treatments of NAFLD.
Keyphrases
  • liver injury
  • drug induced
  • insulin resistance
  • adipose tissue
  • liver fibrosis
  • metabolic syndrome
  • type diabetes
  • oxidative stress
  • fatty acid
  • high fat diet
  • small molecule
  • skeletal muscle