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Cell Death
Bile Acids: The Hidden Gateway Behind Autophagy Modulation in the Liver
In 2016 the Nobel Prize in Physiology or Medicine was awarded to Yoshinori Ohsumi for his discoveries of mechanisms for autophagy. This has been the highest accolade to this field, which started developing 50 years ago when De Duve coined the termed autophagy.1 Since the early birth of this field, autophagy has been linked intimately to liver metabolism. Autophagy is an essential recycling mechanism that ensures an equilibrium between synthesis and degradation of intracellular components. During the 50 years since its first description, autophagy has been shown to be involved in a multitude of cellular processes and degrade very diverse cellular components ranging from organelles, proteins, or glycogen to lipids.Targeting the Enterohepatic Bile Acid Signaling Induces Hepatic Autophagy via a CYP7A1–AKT–mTOR Axis in Mice
Hepatic cholesterol accumulation and autophagy defects contribute to hepatocyte injury in fatty liver disease. Bile acid synthesis is a major pathway for cholesterol catabolism in the liver. This study aims to understand the molecular link between cholesterol and bile acid metabolism and hepatic autophagy activity.Necrosis, Apoptosis, Necroptosis, Pyroptosis: It Matters How Acinar Cells Die During Pancreatitis
Acute pancreatitis is an unpredictable disease. Most patients develop edema of the pancreas and quickly recover whatever the therapy (or lack thereof), but a minority develop severe complications with significant morbidity and mortality. When the disease is studied in experimental animal models,1 to distinguish between the 2 forms, it appears that all processes begin in acinar cells2 but then develop in different directions. The way acinar cells undergo injury and cell death seems to determine the ultimate severity.Necroptosis Is an Important Severity Determinant and Potential Therapeutic Target in Experimental Severe Pancreatitis
Severe acute pancreatitis is characterized by acinar cell death and inflammation. Necroptosis is an aggressive and proinflammatory mode of cell death that can be prevented by necrostatin-1 administration or receptor-interacting protein kinase (RIP3) deletion.Death Receptor-Mediated Cell Death and Proinflammatory Signaling in Nonalcoholic Steatohepatitis
Nonalcoholic fatty liver disease (NAFLD) is becoming a public health problem worldwide. A subset of patients develop an inflammatory disease, nonalcoholic steatohepatitis (NASH), characterized by steatosis, hepatocellular death, macrophage and neutrophil accumulation, and varying stages of fibrosis. Hepatocyte cell death triggers the cellular inflammatory response, therefore reducing cell death may be salutary in the steatohepatitis disease process. Recently, a better understanding of hepatocyte apoptosis in NASH has been obtained and new information regarding other cell death modes such as necroptosis and pyroptosis has been reported.
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