Following liver regeneration after partial hepatectomy, liver grows back 
precisely to its original mass and does not exceed it. The mechanism regulating 
this "hepatostat" is not clear and no exceptions have been found to date. 
Although pathways initiating liver regeneration have been well studied, 
mechanisms involved in the termination of liver regeneration are unclear. Here, 
we report that integrin-linked kinase (ILK) (involved in transmission of the 
extracellular matrix [ECM] signaling by way of integrin receptors) and/or 
hepatic adaptations that ensue following ILK hepatocyte-targeted removal are 
critical for proper termination of liver regeneration. Following partial 
hepatectomy (PHx), mice with a liver-specific ILK ablation (ILK-KO-Liver) 
demonstrate a termination defect resulting in 58% larger liver than their 
original pre-PHx mass. This increase in post-PHx liver mass is due to sustained 
cell proliferation driven in part by increased signaling through hepatocyte 
growth factor (HGF), and the beta-catenin pathway and Hippo kinase pathways.
CONCLUSION: The data indicate that ECM-mediated signaling by way of ILK is 
essential in proper termination of liver regeneration. This is the first 
evidence of a defect leading to impaired termination of regeneration and 
excessive accumulation of liver weight following partial hepatectomy.