دورية
Loss of RAGE prevents chronic intermittent hypoxia-induced nonalcoholic fatty liver disease viablockade of NF-кB pathway
| العنوان: | Loss of RAGE prevents chronic intermittent hypoxia-induced nonalcoholic fatty liver disease viablockade of NF-кB pathway |
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| المؤلفون: | Tan, Haoqu, Hu, Jinfang, Zuo, Wei, Huang, Yun, Cui, Jian, Gong, Fei, Bai, Wei |
| المصدر: | Gene Therapy; 20220101, Issue: Preprints p1-10, 10p |
| مستخلص: | In recent years, receptor for advanced glycation end-products (RAGE) has been documented to induce liver fibrosis and inflammatory reaction. Further, microarray data analysis of this study predicted high expression of RAGE in non-alcoholic fatty liver disease (NAFLD). However, its specific mechanisms remain to be elucidated. Hence, this study is aimed at investigating the mechanistic insights of RAGE in chronic intermittent hypoxia (CIH)-induced NAFLD. ApoE knockout (ApoE−/−) mice were exposed to CIH to induce NAFLD, and primary hepatocytes were also exposed to CIH to mimic in vitro setting. Accordingly, we found that RAGE and NF-κB were upregulated in the liver tissues of CIH-induced NAFLD mice and CIH-exposed hepatocytes. Depleted RAGE attenuated CIH-induced hepatocyte injury, lipid deposition, and inflammation. The relationship between RAGE and NF-κB was analyzed by in silico analysis and correlation analysis. It was demonstrated that knockdown of RAGE inhibited the NF-кB pathway, thus alleviating CIH-induced disorders in hepatocytes. Moreover, in vivo experiments also verified that depletion of RAGE alleviated CIH-induced NAFLD by inhibiting NF-кB pathway. Collectively, loss of RAGE blocked the NF-кB pathway to alleviate CIH-induced NAFLD, therefore, highlighting a potential hepatoprotective target for treating NAFLD. |
| قاعدة البيانات: | Supplemental Index |
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Full Text Finder | تدمد: | 09697128 14765462 |
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| DOI: | 10.1038/s41434-022-00351-4 |