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Updated: Mar 19, 2026

Isolation of Rat Portal Fibroblasts by In situ Liver Perfusion
Published on: June 29, 2012
Portal myofibroblasts connect angiogenesis and fibrosis in liver
Sara Lemoinne1,2, Dominique Thabut1,3, Chantal Housset4,5,6
1Sorbonne Universités, UPMC Univ Paris 06, INSERM, Centre de Recherche Saint-Antoine (CRSA) & Institute of Cardiometabolism and Nutrition (ICAN), F-75012, Paris, France.
Abstract:
Liver fibrogenesis is a dynamic process including quantitative and qualitative changes of the extracellular matrix, of which the most prominent is the deposition of type I collagen. These changes progressively disrupt normal liver architecture and result in cirrhosis formation. In the fibrotic liver, as in all other fibrotic tissues, the extracellular matrix is produced by cells usually characterized by the de novo expression of alpha-smooth muscle actin and known as myofibroblasts. Portal myofibroblasts (PMFs) appear to be critical in pathological angiogenesis, which constantly occurs in advanced liver fibrosis. Whereas the association between angiogenesis and fibrosis during the progression of liver diseases remains to be elucidated, we suggest that collagen-type-XV-alpha1-producing PMFs could provide an important link both by stabilizing newly formed vessels and by forming a scaffold for the deposition of interstitial collagen.
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