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10.1016/j.clinre.2015.05.017 http://scihub22266oqcxt.onion/10.1016/j.clinre.2015.05.017 C4687970!4687970 !26206577     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26206577 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 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\26206577 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Clin+Res+Hepatol+Gastroenterol 2015 ; 39 Suppl 1 (0 1 ): S69-74 Nephropedia Template TP {{tp|p=26206577 |t=2015. Morphogen-related therapeutic targets for liver fibrosis |pdf=|usr=}}{{26206577 }} gab.com Text Morphogen-related therapeutic targets for liver fibrosis JO: Clin Res Hepatol Gastroenterol http://www.kidney.de/pget.php?&tw=1&pmid=26206577 #FOAvip Recent research on hepatic stellate cells (HSCs) has spotlighted the involvement of morphogens in their cell fate determination in liver fibrosis. Temporally and spatially expressed during embryonic development, morphogens are involved in regulation of cell proliferation and differentiation, and tissue patterning. In normal adult liver, morphogens are generally expressed at low levels. However, in liver disease, myofibroblastic HSCs express morphogens such as Wnt, Shh, Necdin, DLK1, and Notch as part of their participation in fibrogenesis and wound healing. Liver regeneration involves cell proliferation and differentiation akin to embryonic liver development where the cells appear to undergo similar fates, and not surprisingly the morphogens are re-activated for the regenerative purpose in adult liver injury. Evidence also points to crosstalk of these morphogens in regulation of HSC fate determination. Genetic ablation or pharmacologic inhibition of morphogens reverts activated HSC to quiescent cells in culture and attenuates progression of hepatic fibrosis. However, positive regulation of liver regeneration by the morphogens needs to be spared. Therapeutically, manipulation of morphogen activities in a cell type and phase-specific manner should offer new modalities for chronic liver disease. Twit Text FOAVip Morphogen-related therapeutic targets for liver fibrosis ????Clin Res Hepatol Gastroenterol http://www.kidney.de/pget.php?&tw=1&pmid=26206577 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26206577 #FOAvip English Wikipedia <ref>{{Cite pmid|26206577 }}</ref> Morphogen-related therapeutic targets for liver fibrosis #MMPMID26206577 Fung E ; Tsukamoto H Clin Res Hepatol Gastroenterol 2015[Sep]; 39 Suppl 1 (0 1 ): S69-74 PMID26206577 show ga Recent research on hepatic stellate cells (HSCs) has spotlighted the involvement of morphogens in their cell fate determination in liver fibrosis. Temporally and spatially expressed during embryonic development, morphogens are involved in regulation of cell proliferation and differentiation, and tissue patterning. In normal adult liver, morphogens are generally expressed at low levels. However, in liver disease, myofibroblastic HSCs express morphogens such as Wnt, Shh, Necdin, DLK1, and Notch as part of their participation in fibrogenesis and wound healing. Liver regeneration involves cell proliferation and differentiation akin to embryonic liver development where the cells appear to undergo similar fates, and not surprisingly the morphogens are re-activated for the regenerative purpose in adult liver injury. Evidence also points to crosstalk of these morphogens in regulation of HSC fate determination. Genetic ablation or pharmacologic inhibition of morphogens reverts activated HSC to quiescent cells in culture and attenuates progression of hepatic fibrosis. However, positive regulation of liver regeneration by the morphogens needs to be spared. Therapeutically, manipulation of morphogen activities in a cell type and phase-specific manner should offer new modalities for chronic liver disease. |Calcium-Binding Proteins [MESH] |Cell Transdifferentiation/physiology [MESH] |Hedgehog Proteins/physiology [MESH] |Hepatic Stellate Cells/physiology [MESH] |Humans [MESH] |Intercellular Signaling Peptides and Proteins/physiology [MESH] |Liver Cirrhosis/*physiopathology [MESH] |Membrane Proteins/physiology [MESH] |Morphogenesis [MESH] |Nerve Tissue Proteins/physiology [MESH] |Nuclear Proteins/physiology [MESH] |Receptors, Notch/physiology [MESH] |Signal Transduction/physiology [MESH]Morphogen-related therapeutic targets for liver fibrosis (epmc).pdf DeepDyve Pubget Overpricing