Hepatic fibrosis and cirrhosis: the (myo)fibroblastic cell subpopulations involved.

The International Journal of Biochemistry & Cell Biology. 2005-09-23; :
DOI: 10.1016/j.biocel.2005.08.021

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1. Int J Biochem Cell Biol. 2006 Feb;38(2):135-51. Epub 2005 Sep 23.

Hepatic fibrosis and cirrhosis: the (myo)fibroblastic cell subpopulations

Guyot C(1), Lepreux S, Combe C, Doudnikoff E, Bioulac-Sage P, Balabaud C,
Desmoulière A.

Author information:
(1)GREF, INSERM E0362, Université Victor Segalen Bordeaux 2, 146, rue
Léo-Saignat, Bordeaux Cedex, F-33076 France.

Fibrosis, defined as the excessive deposition of extracellular matrix in an
organ, is the main complication of chronic liver damage. Its endpoint is
cirrhosis, which is responsible for significant morbidity and mortality. The
accumulation of extracellular matrix observed in fibrosis and cirrhosis is due to
the activation of fibroblasts, which acquire a myofibroblastic phenotype.
Myofibroblasts are absent from normal liver. They are produced by the activation
of precursor cells, such as hepatic stellate cells and portal fibroblasts. These
fibrogenic cells are distributed differently in the hepatic lobule: the hepatic
stellate cells resemble pericytes and are located along the sinusoids, in the
Disse space between the endothelium and the hepatocytes, whereas the portal
fibroblasts are embedded in the portal tract connective tissue around portal
structures (vessels and biliary structures). Differences have been reported
between these two fibrogenic cell populations, in the mechanisms leading to
myofibroblastic differentiation, activation and « deactivation », but confirmation
is required. Second-layer cells surrounding centrolobular veins, fibroblasts
present in the Glisson capsule surrounding the liver, and vascular smooth muscle
cells may also express a myofibroblastic phenotype and may be involved in
fibrogenesis. It is now widely accepted that the various types of lesion (e.g.,
lesions caused by alcohol abuse and viral hepatitis) leading to liver fibrosis
involve specific fibrogenic cell subpopulations. The biological and biochemical
characterisation of these cells is thus essential if we are to understand the
mechanisms underlying the progressive development of excessive scarring in the
liver. These cells also differ in proliferative and apoptotic capacity, at least
in vitro. All this information is required for the development of treatments
specifically and efficiently targeting the cells responsible for the development
of fibrosis/cirrhosis.

DOI: 10.1016/j.biocel.2005.08.021
PMID: 16257564 [Indexed for MEDLINE]

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