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.

中文翻译：

---

REV-ERB激动剂改善NASH小鼠模型的肝脏病理

非酒精性脂肪肝疾病（NAFLD）影响全世界的许多人，目前还没有药物治疗。NAFLD通常表现为肥胖，胰岛素抵抗以及某些情况下的心血管疾病。显然需要缓解该疾病的治疗方案，因为它通常会发展为更加严重的非酒精性脂肪性肝炎（NASH）。REV-ERB核受体是一种转录阻遏物，可调节与NAFLD发育有关的生理过程，包括脂肪形成和炎症。我们假设药理上激活REV-ERB会抑制NASH小鼠模型中脂肪肝的进展。在老鼠NASH模型中使用REV-ERB激动剂SR9009，