A frequent misinterpretation in current research on liver fibrosis: the vessel in the center of CCl-induced pseudolobules is a portal vein.

Abstract

Carbon tetrachloride-induced liver injury is a thoroughly studied model for regeneration and fibrosis in rodents. Nevertheless, its pattern of liver fibrosis is frequently misinterpreted as portal type. To clarify this, we show that collagen type IV"streets" and α-SMAcells accumulate pericentrally and extend to neighbouring central areas of the liver lobule, forming a 'pseudolobule'. Blood vessels in the center of such pseudolobules are portal veins as indicated by the presence of bile duct cells (CK19) and the absence of pericentral hepatocytes (glutamine synthetase). It is critical to correctly describe this pattern of fibrosis, particulary for metabolic zonation studies.