A new collaborative study performed by researchers at the University of Dresden (Germany) and BSRC “Alexander Fleming” (Greece) published in Hepatology identifies a central role of RNA-binding proteins in NAFLD and its progression to HCC.
Non-alcoholic fatty liver disease (NAFLD) is initiated by steatosis and can progress via fibrosis and cirrhosis to hepatocellular carcinoma (HCC). In hepatocytes, the RNA-binding protein Elavl1/HuR -which acts as a central post-transcriptional controller- has been previously implicated in the regulation of diet-induced hepatic steatosis
In a new study entitled “HuR as a gatekeeper of liver homeostasis,” a team of researchers led by T. Chavakis & S. Pallavi at Uni. Dresden and D.L. Kontoyiannis & S. Gargani at Fleming explored the response of hepatocyte-specific HuR-deficient mice to regular and NAFLD-inducing diets. They demonstrate that HuR has a more central role in preventing NAFLD-related fibrosis and HCC. To gain further insight, they coupled lipidomics, transcriptomics, and HuR-RNA interaction screens in the liver. In doing so, they revealed a HuR-dependent network that can be exploited therapeutically since it orchestrates homeostatic metabolic & lipid responses to confer protection; as well as control the fibrotic process.