دورية أكاديمية
Rev-erbα exacerbates hepatic steatosis in alcoholic liver diseases through regulating autophagy
| العنوان: | Rev-erbα exacerbates hepatic steatosis in alcoholic liver diseases through regulating autophagy |
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| المؤلفون: | Qingxue Liu, Lei Xu, Meifei Wu, Yiwen Zhou, Junfa Yang, Cheng Huang, Tao Xu, Jun Li, Lei Zhang |
| المصدر: | Cell & Bioscience, Vol 11, Iss 1, Pp 1-15 (2021) |
| بيانات النشر: | BMC, 2021. |
| سنة النشر: | 2021 |
| المجموعة: | LCC:Biotechnology LCC:Biology (General) LCC:Biochemistry |
| مصطلحات موضوعية: | Rev-erbα, AFL, Autophagy, Bmal1, Lysosome, Biotechnology, TP248.13-248.65, Biology (General), QH301-705.5, Biochemistry, QD415-436 |
| الوصف: | Abstract Background and aims Alcoholic fatty liver (AFL) is a liver disease caused by long-term excessive drinking and is characterized by hepatic steatosis. Understanding the regulatory mechanism of steatosis is essential for the treatment of AFL. Rev-erbα is a member of the Rev-erbs family of nuclear receptors, playing an important role in regulating lipid metabolism. However, its functional role in AFL and its underlying mechanism remains unclear. Results Rev-erbα was upregulated in the liver of EtOH-fed mice and EtOH-treated L-02 cells. Further, Rev-erbα activation exacerbates steatosis in L-02 cells. Inhibition/downexpression of Rev-erbα improved steatosis. Mechanistically, autophagy activity was inhibited in vivo and vitro. Interestingly, inhibition/downexpression of Rev-erbα enhanced autophagy. Furthermore, silencing of Rev-erbα up-regulated the nuclear expression of Bmal1. Autophagy activity was inhibited and steatosis was deteriorated after EtOH-treated L-02 cells were cotransfected with Rev-erbα shRNA and Bmal1 siRNA. Conclusions Rev-erbα induces liver steatosis, which promotes the progression of AFL. Our study reveals a novel steatosis regulatory mechanism in AFL and suggest that Rev-erbα might be a potential therapeutic target for AFL. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 2045-3701 |
| Relation: | https://doaj.org/toc/2045-3701 |
| DOI: | 10.1186/s13578-021-00622-4 |
| URL الوصول: | https://doaj.org/article/e177a0915ea04fd6aa80324be3d165cb |
| رقم الأكسشن: | edsdoj.177a0915ea04fd6aa80324be3d165cb |
| قاعدة البيانات: | Directory of Open Access Journals |
Find this article in full text from Springer Verlag. 
Full Text Finder | تدمد: | 20453701 |
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| DOI: | 10.1186/s13578-021-00622-4 |