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      Mechanisms of bile acid mediated Inflammation in the Liver

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          Abstract

          Bile acids are synthesized in the liver and are the major component in bile. Impaired bile flow leads to cholestasis that is characterized by elevated levels of bile acid in the liver and serum, followed by hepatocyte and biliary injury. Although the causes of cholestasis have been extensively studied, the molecular mechanisms as to how bile acids initiate liver injury remain controversial. In this chapter, we summarize recent advances in the pathogenesis of bile acid induced liver injury. These include bile acid signaling pathways in hepatocytes as well as the response of cholangiocytes and innate immune cells in the liver in both patients with cholestasis and cholestatic animal models. We focus on how bile acids trigger the production of molecular mediators of neutrophil recruitment and the role of the inflammatory response in this pathological process. These advances point to a number of novel targets where drugs might be judged to be effective therapies for cholestatic liver injury.

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          Author and article information

          Journal
          7603128
          5672
          Mol Aspects Med
          Mol. Aspects Med.
          Molecular aspects of medicine
          0098-2997
          1872-9452
          6 July 2017
          01 July 2017
          August 2017
          01 August 2018
          : 56
          : 45-53
          Affiliations
          The Liver Center, Yale University School of Medicine, New Haven, CT 065201
          Author notes
          Address correspondence to: James L. Boyer, MD, Ensign Professor of Medicine, Department of Medicine, Yale University School of Medicine, 333 Cedar Street/1080 LMP, P.O. Box 208019, New Haven, CT 06520-8019. Phone: 203-785-7312; Fax: 203-785-7273; james.boyer@ 123456yale.edu
          Article
          PMC5662014 PMC5662014 5662014 nihpa889921
          10.1016/j.mam.2017.06.001
          5662014
          28606651
          ea890aee-ee90-4a13-b500-6195459a5893
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