Publication: Liver fibrosis, the hepatic stellate cell
and tissue inhibitors of metalloproteinases
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Date
2000
Authors
McCrudden, R. ; Iredale, J. P.
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Liver fibrosis occurs as a consequence of net
accumulation of matrix proteins (especially collagen
types I and III) in response to liver injury. The
pathogenesis of liver fibrosis is underpinned by the
activation of hepatic stellate cells (HSC) to a
myofibroblast like phenotype with a consequent increase
in their synthesis of matrix proteins such as interstitial
collagens that characterise fibrosis. In addition to this
there is increasing evidence that liver fibrosis is a
dynamic pathologic process in which altered matrix
degradation may also playa major role. Extracellular
degradation of matrix proteins is regulated by matrix
metalloproteinases (MMPS) - produced by HSC - which
in turn are regulated by several mechanisms which
include regulation at the level of the gene (transcription
and proenzyme synthesis), cleavage of the proenzyme to
an active form and specific inhibition of activated forms
by tissue inhibitors of metalloproteinases (TIMPS).
Insights gained into the molecular regulation of HSC
activation will lead to therapeutic approaches in
treatment of hepatic fibrosis in the future , and could lead
to reduced morbidity and mortality in patients with
chronic liver injury .
Citation
Histology and Histopathology, Vol. 15, n.º 4 (2000)
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