Published online Mar 27, 2015. doi: 10.4254/wjh.v7.i3.377
Peer-review started: August 28, 2014
First decision: September 19, 2014
Revised: November 10, 2014
Accepted: November 27, 2014
Article in press: November 27, 2014
Published online: March 27, 2015
Processing time: 215 Days and 7.8 Hours
Core tip: Hepatic angiogenesis is closely associated with the progression of fibrosis in chronic liver diseases (CLDs). Recent evidences demonstrated that blocking angiogenesis means also prevention of fibrosis progression. Hypoxia plays a crucial role in eliciting angiogenesis together with hepatic stellate cells being the most prominent sources of vascular endothelial growth factor and Angiopoietin-1. Adipokines, endoplasmic reticulum stress and related unfolded protein response; neuropilins; might be future therapeutical target in the progression of fibrosis in CLDs. Moreover studies on non-alcoholic steatohepatits demonstrated that of angiotensin and renin inhibitors could be effectively used as a new treatment strategy against angiogenesis in the prevention of fibrosis in CLDs.
