Published online Sep 26, 2018. doi: 10.12998/wjcc.v6.i10.335
Peer-review started: May 28, 2018
First decision: July 3, 2018
Revised: July 23, 2018
Accepted: August 3, 2018
Article in press: August 4, 2018
Published online: September 26, 2018
Processing time: 121 Days and 5.1 Hours
Portal hypertension (PHT) is an important consequence of liver cirrhosis, which can lead to complications that adversely affect a patient’s quality of life and survival, such as upper gastrointestinal bleeding, ascites, and portosystemic encephalopathy. In recent years, advances in molecular biology have led to major discoveries in the pathological processes of PHT, including the signaling pathways that may be involved: PI3K-AKT-mTOR, RhoA/Rho-kinase, JAK2/STAT3, and farnesoid X receptor. However, the pathogenesis of PHT is complex and there are numerous pathways involved. Therefore, the targeting of signaling pathways for medical management is lagging. This article summarizes the progress that has been made in understanding the signaling pathways in PHT, and provides ideas for treatment of the disorder.
Core tip: Portal hypertension (PHT) is a syndrome of portal venous system hemodynamics in liver cirrhosis. Current therapeutic options are often insufficient to prevent progression of the disease. We therefore may find more effective clinical treatments by understanding the signal pathways involved in the disease. This paper is an up-to-date and thorough review of the signaling pathways that may be involved in the pathogenesis of PHT in liver cirrhosis.
