A frequent misinterpretation in current research on liver fibrosis: the vessel in the center of CCl4-induced pseudolobules is a portal vein

Arch Toxicol. 2017 Nov;91(11):3689-3692. doi: 10.1007/s00204-017-2040-8. Epub 2017 Aug 19.


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-SMA+ cells 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.

Keywords: CCl4; Liver fibrosis; Pseudolobule.

MeSH terms

  • Actins / metabolism
  • Animals
  • Carbon Tetrachloride / toxicity*
  • Collagen Type IV / metabolism
  • Disease Models, Animal
  • Glutamate-Ammonia Ligase / metabolism
  • Liver Cirrhosis / chemically induced*
  • Liver Cirrhosis / pathology
  • Mice, Inbred C57BL
  • Portal Vein / drug effects*
  • Portal Vein / pathology


  • Actins
  • Collagen Type IV
  • alpha-smooth muscle actin, mouse
  • Carbon Tetrachloride
  • Glutamate-Ammonia Ligase