Journal of Medical Molecular Biology ›› 2024, Vol. 21 ›› Issue (1): 1-8.doi: 10.3870/j.issn.1672-8009.2024.01.001

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Mechanism of Fam172a Gene Knockout Exacerbating Non-alcoholic Fatty Liver Disease #br#

  

  1. 1Department of Gastroenterology, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China 2Department of Gastroenterology, Peking University Ditan Teaching Hospital, Beijing, 100015, China  3Beijing Key Laboratory of Emerging Infectious Diseases, Institute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China 4Beijing Institute of Infectious Diseases, Beijing, 100015, China 5National Center for Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China 6National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, Beijing, 100015, China
  • Online:2024-01-31 Published:2024-03-07

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Abstract: ObjectiveTo explore the mechanism of Fam172a gene knockout in enhancing endoplasmic reticulum stress (ERS) induced nonalcoholic fatty liver disease (NAFLD). Methods Mice were intraperitoneally injected with PBS, tunicamycin ( TM), or the NF-κB inhibitor DHMEQ. The hepatic function and hepatic lipid accumulation were then evaluated, and protein levelswere assessed via Western blotting. Results Compared to the control group, the Fam172a - / - -TMgroup had significantly increased levels of serum ALT and AST, along with the increased liver structure damage and lipid accumulation. Additionally, the relative expression levels of GRP78, CHOP,and pNF-κB / NF-κB in liver tissues were significantly up-regulated in the Fam172a - / - -TM group. Furthermore, DHMEQ significantly reduced liver injury, lipid accumulation, and ERS inFam172a - / - mice. Conclusion Fam172a knockout could enhance the ERS-induced NAFLD byactivation of NF-κB pathway.

Key words:

Fam172a, nonalcoholic fatty liver disease, endoplasmic reticulum stress, nuclear factor kappa B

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