The relationship between apoptosis and non-alcoholic fatty liver disease: An evolutionary cornerstone turned pathogenic

Ali Canbay, R. K. Gieseler, G. J. Gores, G. Gerken

Research output: Contribution to journalReview article

23 Scopus citations

Abstract

The data currently available favor a model for the pathogenesis of non-alcoholic fatty liver disease that is based on an apparent sequential relationship of intrahepatic apoptosis, inflammation and fibrogenesis. Based on both hepatic and peripheral insulin resistance, the hepatocellular accumulation of triglycerides, termed steatosis, initially leads to an altered metabolism of glucose and free fatty acids in the liver. In response, increased expression of death receptors in simple steatosis enhances the hepatocytes' susceptibility for pro-apoptotic stimuli, thus eliciting excessive hepatocyte apoptosis and inflammation. Evidence indicates that these processes, if prolonged, activate both hepatic stellate and Kupffer cells, thus leading to a vicious circle in which apoptosis, inflammation, cellular activation, and collagen deposition are upregulated even further.

Original languageEnglish (US)
Pages (from-to)211-217
Number of pages7
JournalZeitschrift fur Gastroenterologie
Volume43
Issue number2
DOIs
StatePublished - Feb 1 2005

Keywords

  • Apoptosis
  • Development
  • Evolution
  • Fibrosis
  • Inflammation
  • NAFLD
  • NASH

ASJC Scopus subject areas

  • Gastroenterology

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