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Molecules, Systems and Signaling in Liver Injury
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Molecules, Systems and Signaling in Liver Injury

Softcover reprint of the original 1st ed. 2017

Book Details

Format Paperback / Softback
ISBN-10 3319863223
ISBN-13 9783319863221
Edition Softcover reprint of the original 1st ed. 2017
Publisher Springer International Publishing AG
Imprint Springer International Publishing AG
Country of Manufacture GB
Country of Publication GB
Publication Date Aug 12th, 2018
Print length 290 Pages
Ksh 23,400.00
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This essential volume presents comprehensive information on cell death and autophagy in liver diseases, including the role and molecular signaling pathways of cell death in alcohol and non-alcoholic fatty liver disease, bile acids, hepatitis C virus and drug-induced liver injury.
This essential volume presents comprehensive information on cell death and autophagy in liver diseases, including the role and molecular signaling pathways of cell death in alcohol and non-alcoholic fatty liver disease, bile acids, hepatitis C virus and drug-induced liver injury. The book starts with a discussion of lipotoxicity in non-parenchymal cells, followed by a discussion of cell death and autophagy in cholangiocytes, hepatic stellate cells and Kupffer cells in hepatic biliary diseases, fibrosis and liver inflammation. The book also covers Bcl-2 family proteins, beta-catenin and HMGB1 signaling in regulating cell death in the liver as well as mitochondria, ER stress and gut microbiota on liver injury. The Cell Death in Biology and Diseases series has recruited world experts ranging from basic scientists to clinicians on cell death in liver diseases. Likewise the contributors of this volume are leaders in their fields with worldwide expertise and perspective. Molecules, Systems and Signaling in Liver Injury is an essential companion to Hepatocytes and Non-Parenchymal Cells and Diseases. It is beneficial for both clinicians and basic scientists and is relevant to those working on drug discovery for preventing and treating liver diseases by targeting cell death and autophagy pathways.

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