title: Autophagy in alcohol-induced liver diseases.
abstract: Alcohol is the most abused substance worldwide and a significant source of liver injury; the mechanisms of alcohol-induced liver disease are not fully understood. Significant cellular toxicity and impairment of protein synthesis and degradation occur in alcohol-exposed liver cells, along with changes in energy balance and modified responses to pathogens. Autophagy is the process of cellular catabolism through the lysosomal-dependent machinery, which maintains a balance among protein synthesis, degradation, and recycling of self. Autophagy is part of normal homeostasis and it can be triggered by multiple factors that threaten cell integrity, including starvation, toxins, or pathogens. Multiple factors regulate autophagy; survival and preservation of cellular integrity at the expense of inadequately folded proteins and damaged high-energy generating intracellular organelles are prominent targets of autophagy in pathological conditions. Coincidentally, inadequately folded proteins accumulate and high-energy generating intracellular organelles, such as mitochondria, are damaged by alcohol abuse; these alcohol-induced pathological findings prompted investigation of the role of autophagy in the pathogenesis of alcohol-induced liver damage. Our review summarizes the current knowledge about the role and implications of autophagy in alcohol-induced liver disease.
authors.affiliation: Department of Internal Medicine, University of Florida, Gainesville, USA. angela.dolganiuc@medicine.uﬂ.edu
authors.forename: Angela
authors.initials: A
authors.lastname: Dolganiuc
authors.forename: Paul G
authors.initials: PG
authors.lastname: Thomes
authors.forename: Wen-Xing
authors.initials: WX
authors.lastname: Ding
authors.forename: John J
authors.initials: JJ
authors.lastname: Lemasters
authors.forename: Terrence M
authors.initials: TM
authors.lastname: Donohue
mesh_terms: D000818:Animals; D001343:Autophagy / Q000502:physiology*; D015415:Biomarkers; D016923:Cell Death / Q000187:drug effects; D002492:Central Nervous System Depressants / Q000633:toxicity; D004195:Disease Models, Animal; D000431:Ethanol / Q000633:toxicity; D006801:Humans; D008108:Liver Diseases, Alcoholic / Q000473:pathology*; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D010588:Phagosomes / Q000378:metabolism; D011506:Proteins / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D051193:Toll-Like Receptors / Q000187:drug effects
chemical_list: D015415:Biomarkers; D002492:Central Nervous System Depressants; D011506:Proteins; D051193:Toll-Like Receptors; D000431:Ethanol; D058570:TOR Serine-Threonine Kinases