REV-ERB agonism improves liver pathology in a mouse model of NASH.
REV-ERB agonism improves liver pathology in a mouse model of NASH.
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DOI：
10.1371/journal.pone.0236000
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发表时间：
2020
期刊：
影响因子：
3.7
通讯作者：
Burris TP
中科院分区：
文献类型：
--
作者：
Griffett K;Bedia-Diaz G;Elgendy B;Burris TP
非酒精性脂肪性肝病（NAFLD）影响着世界范围内的大量人群，目前尚无药物治疗方法。NAFLD通常表现为肥胖、胰岛素抵抗，在某些情况下还会出现心血管疾病。由于这种疾病常常发展为严重得多的非酒精性脂肪性肝炎（NASH），因此显然需要治疗方案来缓解这种疾病。REV-ERB核受体是一种转录抑制因子，调节涉及NAFLD发展的生理过程，包括脂肪生成和炎症。我们假设药理学激活REV-ERB可以抑制NASH小鼠模型中脂肪肝的进展。在小鼠NASH模型中使用REV-ERB激动剂SR9009，我们证明了REV-ERB激活的有益作用，通过抑制肝纤维化和炎症反应，导致肝脏健康的整体改善。
Non-alcoholic fatty liver disease (NAFLD) affects a significant number of people worldwide and currently there are no pharmacological treatments. NAFLD often presents with obesity, insulin resistance, and in some cases cardiovascular diseases. There is a clear need for treatment options to alleviate this disease since it often progresses to much more the much more severe non-alcoholic steatohepatitis (NASH). The REV-ERB nuclear receptor is a transcriptional repressor that regulates physiological processes involved in the development of NAFLD including lipogenesis and inflammation. We hypothesized that pharmacologically activating REV-ERB would suppress the progression of fatty liver in a mouse model of NASH. Using REV-ERB agonist SR9009 in a mouse NASH model, we demonstrate the beneficial effects of REV-ERB activation that led to an overall improvement of hepatic health by suppressing hepatic fibrosis and inflammatory response.
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LXR反向激动剂SR9238在非酒精性脂肪性肝炎模型中抑制纤维化。
影响因子：
8.1
作者：
Griffett K;Welch RD;Flaveny CA;Kolar GR;Neuschwander-Tetri BA;Burris TP
通讯作者：
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影响因子：
29.4
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影响因子：
3.5
作者：
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通讯作者：
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影响因子：
4
作者：
Griffett, Kristine;Solt, Laura A.;Burris, Thomas P.
通讯作者：
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影响因子：
3.7
作者：
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