RIPK1 protects from TNF-α-mediated liver damage during hepatitis.

ABSTRACT: Cell death of hepatocytes is a prominent characteristic in the pathogenesis of liver disease, while hepatolysis is a starting point of inflammation in hepatitis and loss of hepatic function. However, the precise molecular mechanisms of hepatocyte cell death, the role of the cytokines of hepatic microenvironment and the involvement of intracellular kinases, remain unclear. Tumor necrosis factor alpha (TNF-α) is a key cytokine involved in cell death or survival pathways and the role of RIPK1 has been associated to the TNF-α-dependent signaling pathway. We took advantage of two different deficient mouse lines, the RIPK1 kinase dead knock-in mice (Ripk1^K45A) and the conditional knockout mice lacking RIPK1 only in liver parenchymal cells (Ripk1^LPC-KO), to characterize the

SUBMITTER: Filliol A 

PROVIDER: S-EPMC5260888 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature