Abstract:Mice deficient in the antioxidant enzyme Cu/Zn-superoxide dismutase (Sod1-/- or Sod1KO mice) develop spontaneous hepatocellular carcinoma (HCC) with age. Similar to humans, HCC development in Sod1KO mice progresses from fatty liver disease to non-alcoholic steatohepatitis (NASH) with fibrosis, which eventually progresses to HCC. Because liver inflammation is the main mechanism that drives the disease progression in chronic liver disease (CLD) and because necroptosis is a major source of inflammation, we tested… Show more
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