Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
, 43 (2), 211-7

The Relationship Between Apoptosis and Non-Alcoholic Fatty Liver Disease: An Evolutionary Cornerstone Turned Pathogenic

Affiliations
Review

The Relationship Between Apoptosis and Non-Alcoholic Fatty Liver Disease: An Evolutionary Cornerstone Turned Pathogenic

A Canbay et al. Z Gastroenterol.

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.

Similar articles

See all similar articles

Cited by 7 PubMed Central articles

See all "Cited by" articles

LinkOut - more resources

Feedback