Stellate cells as a central regulator of intracellular signaling<br /> in the process of liver fibrosis
Journal Title: Postępy Nauk Medycznych - Year 2010, Vol 23, Issue 1
Abstract
Hepatic fibrosis represents cellular response to chronic liver injury. It can lead to cirrhosis and organ failure with all their negative consequences – portal hypertension with gastrointestinal bleeding, ascites, coagulopathy, and hepatic encephalopathy. Hepatic stellate cells (HSC) are nonparenchymal, quiescent cells, whose main function is to store vitamin A in normal liver. Upon liver injury they undergo an activation process, which represents a transition into proliferative, fibrogenic, proinflammatory and contractile phenotype. Cross – talk between hepatocytes, Kupffer cells, inflammatory cells and HSC induces profibrogenic signals and triggers fibrogenesis. The ativation of HSC remains a central event in the process of liver fibrosis and can be subdivided into two major phases: 1. initiation, also called pre-inflammatory stage and 2. perpetuation which maintain the activated phenotype of HSC and generate fibrosis. As the injurious agent is removed, the resolution of hepatic fibrosis with the decrease in activated HSC number can occur. Two potential pathways account for this process: 1. reversion to quiescent phenotype or 2. clearance through apoptosis. Research over past 20 years has indicated of HSC involvment not only in liver injury, but also in hepatic development, regeneration, xenobiotic responses and immunoregulation. Progress in this area has elucidated potential possibility of therapeutic intervention that might help patients with chronic liver disease. This review highlights characteristics of biology of hepatic stellate cells and their interaction with other cell types during induction, progession and resolution of liver fibrosis.
Authors and Affiliations
Beata Kasztelan-Szczerbińska, Maria Słomka, Jadwiga Daniluk, Krzysztof Celiński, Halina Cichoż-Lach, Mariusz Szczerbiński, Agnieszka Zwolak, Iwona Jastrzębska
Keywords
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