Published online May 28, 2015. doi: 10.4254/wjh.v7.i9.1154
Peer-review started: January 20, 2015
First decision: February 7, 2015
Revised: February 14, 2015
Accepted: March 30, 2015
Article in press: April 2, 2015
Published online: May 28, 2015
Processing time: 120 Days and 23.6 Hours
Excessive alcohol intake may induce hepatic apoptosis, steatosis, fibrosis, cirrhosis and even cancer. Ethanol-induced activation of general or selective autophagy as mitophagy or lipophagy in hepatocytes is generally considered a prosurvival mechanism. On the other side of the coin, upregulation of autophagy in non-hepatocytes as stellate cells may stimulate fibrogenesis and subsequently induce detrimental effects on the liver. The autophagic response of other non-hepatocytes as macrophages and endothelial cells is unknown yet and needs to be investigated as these cells play important roles in ethanol-induced hepatic steatosis and damage. Selective pharmacological stimulation of autophagy in hepatocytes may be of therapeutic importance in alcoholic liver disease.
Core tip: This short editorial discusses the impact of ethanol-induced upregulation of cytoprotective bulk and selective autophagy as mitophagy or lipohagy on various types of liver cells. While ethanol-induced activation of autophagy in hepatocytes is generally prosurvival mechanism, upregulation of autophagy in non-hepatocytes as stellate cells may stimulate fibrogenesis and subsequently induce detrimental effects on the liver as a whole. The autophagic response of other non-hepatocytes as macrophages and endothelial cells is unknown yet and needs to be investigated as these cells play important roles in ethanol-induced hepatic steatosis and damage.