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. Author manuscript; available in PMC: 2019 Nov 18.
Published in final edited form as: Cell Death Differ. 2019 Apr 15;26(12):2710–2726. doi: 10.1038/s41418-019-0330-9

Fig. 8. Model for the role of cell death in TAK1-deficient LPCs.

Fig. 8

Proposed model for the contribution of hepatocyte apoptosis and bile epithelial cell necroptosis in the development of chronic liver inflammation, regeneration and hepatocarcinogenesis in TAK1LPC-KO mice. The observed cholestasis aggravates inflammation likely by inducing more hepatocyte apoptosis through released bile acid toxicity. Although the role of necroptosis per se is currently unclear, it could regulate the aggressiveness of hepatocarcinogenesis by shaping the inflammatory microenvironment.