This volume has gathered together some of the world’s experts on cell death in liver diseases, covering topics on a variety of types of liver injury. Specifically, the chapters of this volume describe drug and virus-mediated hepatocyte injury, alcohol, lipid and bile acid-induced hepatocyte injury in addition to ischemia-reperfusion-mediated liver injury. The authors link these different types of liver injury to the commonly associated liver inflammation, fibrosis and tumorigenesis. Other topics explored include the various forms of cell death and cell survival pathways that have been identified in the liver, such as apoptosis, necroptosis, pryoptosis and autophagy. This book, along with its companion volume, Molecules, Systems and Signaling in Hepatic Cell Death, provides a thorough and comprehensive discussion on the topic of cell death and liver disease. Cellular Injury in Liver Diseases is an essential addition to the Cell Death in Biology and Diseases series and will appeal to scientists, clinicians and those doing research for drug discovery.

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. Molecul

This volume has gathered together some of the world’s experts on cell death in liver diseases, covering topics on a variety of types of liver injury. Specifically, the chapters of this volume describe drug and virus-mediated hepatocyte injury, alcohol, lipid and bile acid-induced hepatocyte injury in addition to ischemia-reperfusion-mediated liver injury. The authors link these different types of liver injury to the commonly associated liver inflammation, fibrosis and tumorigenesis. Other topics explored include the various forms of cell death and cell survival pathways that have been identified in the liver, such as apoptosis, necroptosis, pryoptosis and autophagy. This book, along with its companion volume, Molecules, Systems and Signaling in Hepatic Cell Death, provides a thorough and comprehensive discussion on the topic of cell death and liver disease. Cellular Injury in Liver Diseases is an essential addition to the Cell Death in Biology and Diseases series and will appeal to scientists, clinicians and those doing research for drug discovery.

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. Molecul