FIND ARTICLE

Volume: 
Issue: 
1
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Hepatic stellate cells play a key role in the development of liver fibrosis that is characterized by a quantitative and qualitative changes in the composition and distribution of the extracellular matrix . Under the influence of the compounds released from damaged hepatocytes and Kupffer cells Browicz - , platelets , white blood cells and endothelial cells , there is a transition ( activation ) stellate cells quiescent cells myofibroblast phenotype . The activated stellate cells lose lipid droplets , the cells proliferate, migrate, and on the circuit płacika synthesize large quantities of extracellular matrix macromolecules , which leads to fibrosis and ultimately to cirrhosis of the liver. While the primary mitogen for stellate cells is PDGF , and TGF -( is the strongest relationship fibrogenny is in the process of activation of these cells and progressive fibrosis of the liver is involved many other substances acting primarily through paracrine and autocrine . After removal of liver can lead to the withdrawal of the early stages of fibrotic tissue upon activation of metalloproteinases secreted by stellate cells , and reduce the number of these cells by apoptosis Fas -activated receptor . Inhibition of stellate cell activation signal transduction pathways involved in the profibrogenic may prove useful in the future for the treatment of liver fibrosis.

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The Editorial Board
Andrzej Łukaszyk - przewodniczący, Zofia Bielańska-Osuchowska, Szczepan Biliński, Mieczysław Chorąży, Aleksander Koj, Włodzimierz Korochoda, Leszek Kuźnicki, Aleksandra Stojałowska, Lech Wojtczak

Editorial address:
Katedra i Zakład Histologii i Embriologii Uniwersytetu Medycznego w Poznaniu, ul. Święcickiego 6, 60-781 Poznań, tel. +48 61 8546453, fax. +48 61 8546440, email: mnowicki@ump.edu.pl

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