{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mohammed S"],"funding":["BLRD VA","NIA NIH HHS","Oklahoma Center for the Advancement of Science and Technology","Presbyterian Health Foundation","U.S. Department of Veterans Affairs","National Institute on Aging"],"pagination":["315-328"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8845573"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["164"],"pubmed_abstract":["Mice deficient in the antioxidant enzyme Cu/Zn-superoxide dismutase (Sod1<sup>-/-</sup> or Sod1KO mice) have increased oxidative stress, show accelerated aging and develop spontaneous hepatocellular carcinoma (HCC) with age. Similar to humans, HCC development in Sod1KO mice progresses from non-alcoholic fatty liver disease (NAFLD) to non-alcoholic steatohepatitis (NASH) with fibrosis, which eventually progresses to HCC. Oxidative stress plays a role in NAFLD to NASH progression, and liver inflammation is the main mechanism that drives the disease progression from NASH to fibrosis. Because necroptosis is a major source of inflammation, we tested the hypothesis that increased necroptosis in the liver plays a role in increased inflammation and fibrosis in Sod1KO mice. Phosphorylation of MLKL "],"journal":["Free radical biology & medicine"],"pubmed_title":["Role of necroptosis in chronic hepatic inflammation and fibrosis in a mouse model of increased oxidative stress."],"pmcid":["PMC8845573"],"funding_grant_id":["P30 AG050911","R01 AG059718","IK6 BX005238","R01 AG057424","I01 BX004538"],"pubmed_authors":["Nicklas EH","Richardson A","Thadathil N","Kinter M","Mohammed S","Selvarani R","Royce GH","Deepa SS"],"additional_accession":[]},"is_claimable":false,"name":"Role of necroptosis in chronic hepatic inflammation and fibrosis in a mouse model of increased oxidative stress.","description":"Mice deficient in the antioxidant enzyme Cu/Zn-superoxide dismutase (Sod1<sup>-/-</sup> or Sod1KO mice) have increased oxidative stress, show accelerated aging and develop spontaneous hepatocellular carcinoma (HCC) with age. Similar to humans, HCC development in Sod1KO mice progresses from non-alcoholic fatty liver disease (NAFLD) to non-alcoholic steatohepatitis (NASH) with fibrosis, which eventually progresses to HCC. Oxidative stress plays a role in NAFLD to NASH progression, and liver inflammation is the main mechanism that drives the disease progression from NASH to fibrosis. Because necroptosis is a major source of inflammation, we tested the hypothesis that increased necroptosis in the liver plays a role in increased inflammation and fibrosis in Sod1KO mice. Phosphorylation of MLKL ","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Feb","modification":"2025-04-04T14:58:47.538Z","creation":"2025-04-04T14:58:47.538Z"},"accession":"S-EPMC8845573","cross_references":{"pubmed":["33429022"],"doi":["10.1016/j.freeradbiomed.2020.12.449"]}}