RT Journal Article
SR Electronic
T1 REV-ERB Agonism Improves Liver Pathology in a Mouse Model of NASH
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.06.29.177378
DO 10.1101/2020.06.29.177378
A1 Kristine Griffett
A1 Gonzalo Bedia-Diaz
A1 Bahaa El-Dien M. Elgendy
A1 Thomas P. Burris
YR 2020
UL http://biorxiv.org/content/early/2020/06/29/2020.06.29.177378.abstract
AB 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 lipogenesis and inflammation.