Published online May 21, 2017. doi: 10.3748/wjg.v23.i19.3396
Peer-review started: February 8, 2017
First decision: March 3, 2017
Revised: March 17, 2017
Accepted: April 12, 2017
Article in press: April 12, 2017
Published online: May 21, 2017
Processing time: 111 Days and 20.1 Hours
In the last three decades, the understanding of the renin angiotensin system (RAS) has been changed by the discoveries of functional local systems, novel biologically active peptides, additional specific receptors, alternative pathways of angiotensin (Ang) II generation, and new roles for enzymes and precursor components other than those in Ang II synthesis. In this regard, the discovery that Ang-(1-7) opposes the pressor, proliferative, pro-fibrotic, and pro-inflammatory effects mediated by Ang II has contributed to the realization that the RAS is composed of two axes. The first axis consists of the angiotensin-converting enzyme (ACE), with Ang II as the end product, and the angiotensin type 1 (AT1) receptor as the main effector mediating the biological actions of Ang II. The second axis results from ACE2-mediated hydrolysis of Ang II, leading to the production of Ang-(1-7), with the Mas receptor as the main effector conveying the vasodilatory, anti-proliferative, anti-fibrotic, and anti-inflammatory effects of Ang-(1-7). Experimental and clinical studies have shown that both axes of the RAS may take part in the pathogenesis of liver diseases. In this manuscript, we summarize the current evidence regarding the role of RAS in hepatic cirrhosis and its complications, including hemodynamic changes and hepatorenal syndrome. The therapeutic potential of the modulation of RAS molecules in liver diseases is also discussed.
Core tip: This Editorial reports recent advances on the understanding of the renin angiotensin system in regard to the role of the two main and counter-regulatory mediators, Angiotensin II and Angiotensin-(1-7), in liver diseases and in their main complications. Experimental and clinical findings so far show that Angiotensin-(1-7) by binding to Mas receptor opposes Angiotensin II actions mediated by AT1 receptors in liver tissue, by eliciting anti-inflammatory, anti-oxidative and anti-fibrotic effects. This knowledge may help in paving the way for the development of novel treatments for liver diseases and their complications.