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|Title:||Fibroinflammatory Liver Injuries as Preneoplastic Condition in Cholangiopathies||Authors:||Cannito, Stefania
|Keywords:||Caroli’s disease;cholangiocarcinoma;cholangiocytes;neoplastic transformation;primary sclerosing cholangitis||Keywords Plus:||HEPATIC STELLATE CELLS;POLYCYSTIC KIDNEY-DISEASE;TISSUE GROWTH-FACTOR;PRIMARY SCLEROSING CHOLANGITIS;PRIMARY BILIARY-CIRRHOSIS;DUCTULAR REACTION;INTRAHEPATIC CHOLANGIOCARCINOMA;FACTOR-BETA;ANIMAL-MODELS;MOUSE CHOLANGIOCYTES||Mesh headings:||Bile Duct Diseases;Liver;Liver Cirrhosis;Precancerous Conditions||Secondary Mesh headings:||Animals;Epithelium;Humans;Mesoderm||Issue Date:||4-Dec-2018||Publisher:||MDPI||Journal:||International journal of molecular sciences||Abstract:||
The cholangipathies are a class of liver diseases that specifically affects the biliary tree. These pathologies may have different etiologies (genetic, autoimmune, viral, or toxic) but all of them are characterized by a stark inflammatory infiltrate, increasing overtime, accompanied by an excess of periportal fibrosis. The cellular types that mount the regenerative/reparative hepatic response to the damage belong to different lineages, including cholagiocytes, mesenchymal and inflammatory cells, which dynamically interact with each other, exchanging different signals acting in autocrine and paracrine fashion. Those messengers may be proinflammatory cytokines and profibrotic chemokines (IL-1, and 6; CXCL1, 10 and 12, or MCP-1), morphogens (Notch, Hedgehog, and WNT/β-catenin signal pathways) and finally growth factors (VEGF, PDGF, and TGFβ, among others). In this review we will focus on the main molecular mechanisms mediating the establishment of a fibroinflammatory liver response that, if perpetuated, can lead not only to organ dysfunction but also to neoplastic transformation. Primary Sclerosing Cholangitis and Congenital Hepatic Fibrosis/Caroli's disease, two chronic cholangiopathies, known to be prodrome of cholangiocarcinoma, for which several murine models are also available, were also used to further dissect the mechanisms of fibroinflammation leading to tumor development.
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