Effects of hepatic mARC1 inhibition in a mouse model of liver fibrosis

Despite the high prevalence of the disease, there are currently few treatment options in part because the mechanistic basis causative to hepatic fatty acid biogenesis and accumulation are unresolved. Recent evidence indicates that enhanced mitochondrial amidoxime-reducing component 1 (mARC1) induction is associated with increased hepatic triglyceride accumulation and reduced plasma triglycerides indicting that it may play an important role in NASH pathogenesis.

The goal of this study is to explore the therapeutic potential of mARC1 inhibition on the inhibition or reversal of NASH pathogenesis in a mouse model of diet induced MASH.