Poster overview:

The human liver and gut are uniquely linked and play a crucial role in controlling the pathology of the liver. It has been proposed that changes in this gut-liver axis is tightly linked with the progression of non-alcoholic fatty liver disease (NAFLD) into non-alcoholic steatohepatitis (NASH).

As there are currently no FDA-approved drugs for the treatment of NAFLD/NASH, there is a clear requirement to better understand the mechanisms that drive disease progression to better inform therapeutic R&D programs. Unfortunately, traditional in vivo and in vitro preclinical models of NAFLD and NASH suffer from shortfalls that limit their predictability. No one model can fully recapitulate the key aspects of NAFLD/NASH. Moreover, very few accurately capture the human gut-liver axis and enable studies into the molecular mechanisms that drive NAFLD progression.

Here, we demonstrate the potential of  a liver and a gut/liver microphysiological systems (MPS) to recapitulate NAFLD and NASH phenotypes in vitro and explore the molecular mechanisms underlying the development of NAFLD/NASH as well as assess the efficacy of novel therapeutic strategies.

Authors