RIPK1 in Liver Parenchymal Cells Limits Murine Hepatitis during Acute CCl₄-Induced Liver Injury.

ABSTRACT: Some life-threatening acute hepatitis originates from drug-induced liver injury (DILI). Carbon tetrachloride (CCl₄)-induced acute liver injury in mice is the widely used model of choice to study acute DILI, which pathogenesis involves a complex interplay of oxidative stress, necrosis, and apoptosis. Since the receptor interacting protein kinase-1 (RIPK1) is able to direct cell fate towards survival or death, it may potentially affect the pathological process of xenobiotic-induced liver damage. Two different mouse lines, either deficient for Ripk1 specifically in liver parenchymal cells (Ripk1^LPC-KO) or for the kinase activity of RIPK1 (Ripk1^K45A, kinase dead), plus their respective wild-type littermates (Ripk1^fl/fl,

SUBMITTER: Hameed H 

PROVIDER: S-EPMC9266426 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature