Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1016/j.addr.2017.05.007 http://scihub22266oqcxt.onion/10.1016/j.addr.2017.05.007 28506744!5682243!28506744     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28506744&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       Adv+Drug+Deliv+Rev 2017 ; 121 (?): 27-42 Nephropedia Template TP {{tp|p=28506744|t=2017. Hepatic stellate cells as key target in liver fibrosis |pdf=|usr=}}{{28506744}} gab.com Text Hepatic stellate cells as key target in liver fibrosis JO: Adv Drug Deliv Rev http://www.kidney.de/pget.php?&tw=1&pmid=28506744 #FOAvip Progressive liver fibrosis, induced by chronic viral and metabolic disorders, leads to more than one million deaths annually via development of cirrhosis, although no antifibrotic therapy has been approved to date. Transdifferentiation (or "activation") of hepatic stellate cells is the major cellular source of matrix protein-secreting myofibroblasts, the major driver of liver fibrogenesis. Paracrine signals from injured epithelial cells, fibrotic tissue microenvironment, immune and systemic metabolic dysregulation, enteric dysbiosis, and hepatitis viral products can directly or indirectly induce stellate cell activation. Dysregulated intracellular signaling, epigenetic changes, and cellular stress response represent candidate targets to deactivate stellate cells by inducing reversion to inactivated state, cellular senescence, apoptosis, and/or clearance by immune cells. Cell type- and target-specific pharmacological intervention to therapeutically induce the deactivation will enable more effective and less toxic precision antifibrotic therapies. Twit Text FOAVip Hepatic stellate cells as key target in liver fibrosis ????Adv Drug Deliv Rev http://www.kidney.de/pget.php?&tw=1&pmid=28506744 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28506744 #FOAvip English Wikipedia <ref>{{Cite pmid|28506744}}</ref> Hepatic stellate cells as key target in liver fibrosis #MMPMID28506744 Higashi T; Friedman SL; Hoshida Y Adv Drug Deliv Rev 2017[Nov]; 121 (?): 27-42 PMID28506744show ga Progressive liver fibrosis, induced by chronic viral and metabolic disorders, leads to more than one million deaths annually via development of cirrhosis, although no antifibrotic therapy has been approved to date. Transdifferentiation (or "activation") of hepatic stellate cells is the major cellular source of matrix protein-secreting myofibroblasts, the major driver of liver fibrogenesis. Paracrine signals from injured epithelial cells, fibrotic tissue microenvironment, immune and systemic metabolic dysregulation, enteric dysbiosis, and hepatitis viral products can directly or indirectly induce stellate cell activation. Dysregulated intracellular signaling, epigenetic changes, and cellular stress response represent candidate targets to deactivate stellate cells by inducing reversion to inactivated state, cellular senescence, apoptosis, and/or clearance by immune cells. Cell type- and target-specific pharmacological intervention to therapeutically induce the deactivation will enable more effective and less toxic precision antifibrotic therapies. |Animals[MESH] |Hepatic Stellate Cells/*drug effects/metabolism/pathology[MESH] |Humans[MESH] |Liver Cirrhosis/*drug therapy/metabolism/*pathology[MESH]Hepatic stellate cells as key target in liver fibrosis (epmc).pdf DeepDyve Pubget Overpricing