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World J Hepatol. Mar 27, 2015; 7(3): 377-391
Published online Mar 27, 2015. doi: 10.4254/wjh.v7.i3.377
Angiogenesis and liver fibrosis
Gülsüm Özlem Elpek
Gülsüm Özlem Elpek, Department of Pathology, Akdeniz University Medical School, 07070 Antalya, Turkey
Author contributions: Elpek GO solely analyzed the data and wrote the paper.
Conflict-of-interest: The authors declare that they have no competing interests.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Correspondence to: Gülsüm Özlem Elpek, MD, Professor, Department of Pathology, Akdeniz University Medical School, Dumlupınar Bulvarı, 07070 Antalya, Turkey.
Telephone: +90-242-2496389 Fax: +90-242-2275540
Received: August 28, 2014
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
Core Tip

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.