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10.3389/fmed.2015.00072 http://scihub22266oqcxt.onion/10.3389/fmed.2015.00072 C4594310!4594310 !26501061     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26501061 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Med+(Lausanne) 2015 ; 2 (ä): 72 Nephropedia Template TP {{tp|p=26501061 |t=2015. Targeted Therapies in Liver Fibrosis: Combining the Best Parts of Platelet-Derived Growth Factor BB and Interferon Gamma |pdf=|usr=}}{{26501061 }} gab.com Text Targeted Therapies in Liver Fibrosis: Combining the Best Parts of Platelet-Derived Growth Factor BB and Interferon Gamma JO: Front Med (Lausanne) http://www.kidney.de/pget.php?&tw=1&pmid=26501061 #FOAvip Cytokines, growth factors, and other locally produced mediators play key roles in the regulation of disease progression. During liver fibrosis, these mediators orchestrate the balance between pro- and antifibrotic activities as exerted by the hepatic cells. Two important players in this respect are the profibrotic mediator platelet-derived growth factor BB (PDGF-BB) and the antifibrotic cytokine interferon gamma (IFN?). PDGF-BB, produced by many resident and infiltrating cells, causes extensive proliferation, migration, and contraction of hepatic stellate cells (HSCs) and myofibroblasts. These cells are the extracellular matrix-producing hepatic cells and they highly express the PDGF? receptor. On the other hand, IFN? is produced by natural killer cells in fibrotic livers and is endowed with proinflammatory, antiviral, and antifibrotic activities. This cytokine attracted much attention as a possible therapeutic compound in fibrosis. However, clinical trials yielded disappointing results because of low efficacy and adverse effects, most likely related to the dual role of IFN? in fibrosis. In our studies, we targeted the antifibrotic IFN? to the liver myofibroblasts. For that, we altered the cell binding properties of IFN?, by delivery of the IFN?-nuclear localization sequence to the highly expressed PDGF? receptor using a PDGF? receptor recognizing peptide, thereby creating a construct referred to as "Fibroferon" (i.e., fibroblast-targeted interferon ?). In recent years, we demonstrated that HSC-specific delivery of IFN? increased its antifibrotic potency and improved its general safety profile in vivo, making Fibroferon highly suitable for the treatment of (fibrotic) diseases associated with elevated PDGF? receptor expression. The present review summarizes the knowledge on these two key mediators, PDGF-BB and IFN?, and outlines how we used this knowledge to create the cell-specific antifibrotic compound Fibroferon containing parts of both of these mediators. Twit Text FOAVip Targeted Therapies in Liver Fibrosis: Combining the Best Parts of Platelet-Derived Growth Factor BB and Interferon Gamma ????Front Med (Lausanne) http://www.kidney.de/pget.php?&tw=1&pmid=26501061 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26501061 #FOAvip English Wikipedia <ref>{{Cite pmid|26501061 }}</ref> Targeted Therapies in Liver Fibrosis: Combining the Best Parts of Platelet-Derived Growth Factor BB and Interferon Gamma #MMPMID26501061 van Dijk F ; Olinga P ; Poelstra K ; Beljaars L Front Med (Lausanne) 2015[]; 2 (ä): 72 PMID26501061 show ga Cytokines, growth factors, and other locally produced mediators play key roles in the regulation of disease progression. During liver fibrosis, these mediators orchestrate the balance between pro- and antifibrotic activities as exerted by the hepatic cells. Two important players in this respect are the profibrotic mediator platelet-derived growth factor BB (PDGF-BB) and the antifibrotic cytokine interferon gamma (IFN?). PDGF-BB, produced by many resident and infiltrating cells, causes extensive proliferation, migration, and contraction of hepatic stellate cells (HSCs) and myofibroblasts. These cells are the extracellular matrix-producing hepatic cells and they highly express the PDGF? receptor. On the other hand, IFN? is produced by natural killer cells in fibrotic livers and is endowed with proinflammatory, antiviral, and antifibrotic activities. This cytokine attracted much attention as a possible therapeutic compound in fibrosis. However, clinical trials yielded disappointing results because of low efficacy and adverse effects, most likely related to the dual role of IFN? in fibrosis. In our studies, we targeted the antifibrotic IFN? to the liver myofibroblasts. For that, we altered the cell binding properties of IFN?, by delivery of the IFN?-nuclear localization sequence to the highly expressed PDGF? receptor using a PDGF? receptor recognizing peptide, thereby creating a construct referred to as "Fibroferon" (i.e., fibroblast-targeted interferon ?). In recent years, we demonstrated that HSC-specific delivery of IFN? increased its antifibrotic potency and improved its general safety profile in vivo, making Fibroferon highly suitable for the treatment of (fibrotic) diseases associated with elevated PDGF? receptor expression. The present review summarizes the knowledge on these two key mediators, PDGF-BB and IFN?, and outlines how we used this knowledge to create the cell-specific antifibrotic compound Fibroferon containing parts of both of these mediators. äTargeted Therapies in Liver Fibrosis: Combining the Best Parts of Pl(epmc).pdf DeepDyve Pubget Overpricing