MLKL in liver parenchymal cells promotes liver cancer in murine metabolic dysfunction-associated steatotic liver disease.

ABSTRACT: The rising prevalence of hepatocellular carcinoma (HCC) in the last decade is mostly attributable to the growing epidemic of metabolic dysfunction-associated steatotic liver diseases (MASLD). However, the transition from steatosis to steatohepatitis (MASH) and ultimately to HCC is not fully understood. As an executioner protein of necroptosis, the mixed-lineage kinase domain-like protein (MLKL) has been proposed to contribute to MASH and HCC development. To investigate its role in disease progression, mice whose liver parenchymal cells (LPCs) no longer expressed MLKL (Mlkl^LPC-KO) were compared to their control counterparts (Mlkl^fl/fl) using an experimental model combining diabetes induction and a high-fat high-sugar diet (HFHSD) for 4, 8, or 12 weeks. Notably, HFHSD f

SUBMITTER: Imerzoukene G 

PROVIDER: S-EPMC12920736 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature