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• W2623365046 endingPage "655" @default.
• W2623365046 startingPage "643" @default.
• W2623365046 abstract "In homozygous ZZ alpha-1-antitrypsin (AAT) deficiency, the liver synthesizes large quantities of AAT mutant Z, which folds improperly during biogenesis and is retained within the hepatocytes and directed into intracellular proteolysis pathways. These intracellular polymers trigger an injury cascade, which can lead to liver injury. This is highly variable and not all patients develop liver disease. Although not fully described, there is likely a strong influence of genetic and environmental modifiers of the injury cascade and of the fibrotic response. With improved understanding of liver injury mechanisms, new strategies for treatment are now being explored." @default.
• W2623365046 created "2017-06-15" @default.
• W2623365046 creator A5024156994 @default.
• W2623365046 creator A5044001788 @default.
• W2623365046 date "2018-11-01" @default.
• W2623365046 modified "2023-09-29" @default.
• W2623365046 title "Alpha-1-Antitrypsin Deficiency Liver Disease" @default.
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• W2623365046 doi "https://doi.org/10.1016/j.cld.2018.06.010" @default.
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• W2623365046 hasPublicationYear "2018" @default.
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