There are two events in which the<unk>  has the capability to regenerate, one being a partial hepatectomy and the other being damage to the<unk>  by toxins or infection. Damage to<unk>  can also be caused by not having a healthy diet and exercise. The processes described below deal with the pathways triggered after a partial hepatectomy. Following the event of partial hepatectomy, there are three phases for the process of<unk> . The first phase is the priming phase and during this portion, hundreds of genes are activated and prepare the<unk>  for<unk> . This priming phase occurs within 0-5 hours after the hepatectomy and deals mainly with events prior to entering the cell cycle and ensuring that hepatocytes can maintain their homeostatic functions. The second phase deals with the activation of various growth factors such as EGFR (epidermal growth factor receptor) and c-Met. These two factors are major components of<unk> . The final phase deals with termination of proliferation by TGF-β (transforming growth factor beta). Immediately after a hepatectomy, there is an activation of numerous signaling pathways that start the process of<unk> . The first being an increase in urokinase activity. Urokinase is known to activate matrix remodeling. This remodeling causes the release of HGF (hepatic growth factor) and from this release now c-Met can also be activated. EGFR is also activated in the same way as c-Met, and these two growth factors play a major role in the<unk>  process. These processes occur outside of the hepatocyte and prime the<unk>  for<unk> . Once these processes are complete, hepatocytes are able to enter the<unk>  to start the process of proliferation. This is because there is a communication between β-catenin (inside the hepatocyte) and the growth factors of EGFR and c-Met (outside the hepatocyte). This communication can occur because of β-catenin and Notch-1 move to the nucleus of the hepatocyte approximately 15-30 minutes after the hepatectomy. The presence of these two proteins increases the regenerative response and the HGF and EGFR act as direct mitogens and can produce a strong mitogenic response for the hepatocytes to proliferate. After the<unk>  process has completed, TGF-β puts an end to the proliferation by inducing apoptosis. TGFβ1 inhibits the proliferation of hepatocytes by repressing HGF. As mentioned above, urokinase activated the release of HGF; therefore, TGFβ1 also represses the urokinase activity. This process is able to bring the hepatocytes back into their quiescent state. Sometimes, hepatocytes do not have the ability to proliferate and an alternative form of<unk>  is able to take place to rebuild the<unk> . This can happen with the help of biliary epithelial cells having the capability of turning into hepatocytes when the original hepatocytes have problems proliferating. This is due to the fact that biliary cells have two functions, one being the normal transport of bile and the other becoming stem cells for hepatocytes. The same also occurs vice versa, with hepatocytes being able to turn into biliary cells when they cannot proliferate. Both of these kinds of cells are facultative stem cells for each other. Facultative stem cells originally have one fate but upon injury of another type of cell, can function as a stem cell. These two types of cells can repair<unk>  tissue even when the normal mechanism of<unk>  fails.
Liver regeneration
Hepatoprotection
Drug detoxification
Transplant rejection
Carcinogenesis
Lipolysis
Heavy metal detoxification
Renal compensation