Autophagy in Alcohol-Induced Liver Diseases

Angela Dolganiuc, Paul G Thomes, Wen Xing Ding, John J. Lemasters, Terrence Donohue

Research output: Contribution to journalReview article

66 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1301-1308
Number of pages8
JournalAlcoholism: Clinical and Experimental Research
Volume36
Issue number8
DOIs
StatePublished - Aug 1 2012

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Keywords

  • Atg
  • Damage
  • Ethanol
  • Liver
  • Mechanisms
  • Mitophagy
  • Toll-like receptors
  • mTOR

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Toxicology
  • Psychiatry and Mental health

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