Ethanol-induced oxidant stress modulates hepatic autophagy and proteasome activity

Research output: Contribution to journalReview article

29 Citations (Scopus)

Abstract

In this review, we describe research findings on the effects of alcohol exposure on two major catabolic systems in liver cells: the ubiquitin-proteasome system (UPS) and autophagy. These hydrolytic systems are not unique to liver cells; they exist in all eukaryotic tissues and cells. However, because the liver is the principal site of ethanol metabolism, it sustains the greatest damage from heavy drinking. Thus, the focus of this review is to specifically describe how ethanol oxidation modulates the activities of the UPS and autophagy and the mechanisms by which these changes contribute to the pathogenesis of alcohol-induced liver injury. Here, we describe the history and the importance of cellular hydrolytic systems, followed by a description of each catabolic pathway and the differential modulation of each by ethanol exposure. Overall, the evidence for an involvement of these catabolic systems in the pathogenesis of alcoholic liver disease is quite strong. It underscores their importance, not only as effective means of cellular recycling and eventual energy generation, but also as essential components of cellular defense.

Original languageEnglish (US)
Pages (from-to)29-39
Number of pages11
JournalRedox Biology
Volume3
DOIs
StatePublished - Nov 1 2014

Fingerprint

Autophagy
Proteasome Endopeptidase Complex
Oxidants
Liver
Ethanol
Ubiquitin
Alcohols
Alcoholic Liver Diseases
Recycling
Eukaryotic Cells
Drinking
Metabolism
History
Modulation
Tissue
Wounds and Injuries
Oxidation
Research

Keywords

  • Autophagy
  • Ethanol
  • Proteopathy
  • Steatosis
  • Ubiquitin proteasome

ASJC Scopus subject areas

  • Organic Chemistry
  • Clinical Biochemistry

Cite this

Ethanol-induced oxidant stress modulates hepatic autophagy and proteasome activity. / Donohue, Terrence; Thomes, Paul G.

In: Redox Biology, Vol. 3, 01.11.2014, p. 29-39.

Research output: Contribution to journalReview article

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