We challenged hepatocyte-specific Keap1 knockout mice with two different models of non-alcoholic steatohepatitis.
Lack of Keap1 resulted in reduced liver steatosis via inhibition of lipogenesis and enhanced mitochondrial functionality.
Hepatocyte-specific Keap1 deletion significantly decreased apoptotic cell death.
Hepatocyte-specific Keap1 deletion did not attenuate hepatic inflammation and fibrosis.