Liver Progenitor Cells

Liver regeneration occurs through two main mechanisms: the replication and division of mature hepatocytes during moderate liver injury and, in severe liver injury in which hepatocyte replication is impaired, the LPC compartment expands to regenerate the liver (Best et al. 2015). During chronic liver injury, macrophages and NK cells initiate LPC expansion by activating the NF-kB pathway through TNF- like weak inducer of apoptosis (TWEAK) signaling (Dwyer et al. 2014). Ductular reactions appear in the periportal regions and contain liver progenitor regions with increased TWEAK signaling and LPC expansion that correlates with the severity of fibrosis (Williams et al. 2014). LPCs have roles in chronic liver disease (Lanthier et al. 2013), fatty liver disease (Chiba et al. 2011; Richardson et al. 2007), chronic viral hepatitis (Clouston et al. 2005; Libbrecht et al. 2000; Wu et al. 2008) and alcohol-related liver disease (Lowes et al. 1999; Sancho-Bru et al. 2012). In chronic liver disease, the high proliferation rate of LPCs is linked to HCC development (Dumble et al. 2002; Fang et al. 2004). It is important to understand that there is no clear consensus on the mechanism of progenitor cell repair. Some argue that during liver injury in which hepatocyte replication is impaired, small progenitor cells present in the liver have the ability to generate significant number of mature hepatocyte and bile duct cells as well as expressing markers of stem cells (Huch et al. 2013; Lu et al. 2015). On the other hand, other researchers argue against the potency of LPCs as they are unable to generate hepatocytes (Grompe 2014; Schaub et al. 2014).

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