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10.1007/s40495-017-0085-2 http://scihub22266oqcxt.onion/10.1007/s40495-017-0085-2 C5624538!5624538!28983452     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Curr+Pharmacol+Rep 2017 ; 3 (2): 92-100 Nephropedia Template TP {{tp|p=28983452|t=2017. Role of FXR in Liver Inflammation during Nonalcoholic Steatohepatitis |pdf=|usr=}}{{28983452}} gab.com Text Role of FXR in Liver Inflammation during Nonalcoholic Steatohepatitis JO: Curr Pharmacol Rep http://www.kidney.de/pget.php?&tw=1&pmid=28983452 #FOAvip Purpose of review: About 15?25% of patients with simple steatosis of non-alcoholic fatty liver disease progresses to non-alcoholic steatohepatitis (NASH), and the underlying mechanism for this progression has not been elucidated. NASH ultimately could progress to cirrhosis, an irreversible condition. Recent findings: Farnesoid X receptor (FXR) has been studied for its role in modulating inflammation, and the expression of FXR is down-regulated during NASH development. FXR deficiency has shown to progress and exacerbate NASH development, and FXR activation has been protective against liver inflammation associated with NASH. The expression of factors in both the adaptive and innate immune response in the liver are regulated in a FXR-dependent and -independent manner. Summary: Therefore, understanding key signaling pathways of liver inflammation in NASH is important to determine essential components that predispose, progress, or exacerbate NASH. FXR has been identified as a therapeutic target for NASH to prevent liver inflammation. Twit Text FOAVip Role of FXR in Liver Inflammation during Nonalcoholic Steatohepatitis ????Curr Pharmacol Rep http://www.kidney.de/pget.php?&tw=1&pmid=28983452 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28983452 #FOAvip English Wikipedia <ref>{{Cite pmid|28983452}}</ref> Role of FXR in Liver Inflammation during Nonalcoholic Steatohepatitis #MMPMID28983452 Armstrong LE; Guo GL Curr Pharmacol Rep 2017[Apr]; 3 (2): 92-100 PMID28983452show ga Purpose of review: About 15?25% of patients with simple steatosis of non-alcoholic fatty liver disease progresses to non-alcoholic steatohepatitis (NASH), and the underlying mechanism for this progression has not been elucidated. NASH ultimately could progress to cirrhosis, an irreversible condition. Recent findings: Farnesoid X receptor (FXR) has been studied for its role in modulating inflammation, and the expression of FXR is down-regulated during NASH development. FXR deficiency has shown to progress and exacerbate NASH development, and FXR activation has been protective against liver inflammation associated with NASH. The expression of factors in both the adaptive and innate immune response in the liver are regulated in a FXR-dependent and -independent manner. Summary: Therefore, understanding key signaling pathways of liver inflammation in NASH is important to determine essential components that predispose, progress, or exacerbate NASH. FXR has been identified as a therapeutic target for NASH to prevent liver inflammation. äRole of FXR in Liver Inflammation during Nonalcoholic Steatohepatitis (epmc).pdf DeepDyve Pubget Overpricing