©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 14, 2024; 30(18): 2391-2396
Published online May 14, 2024. doi: 10.3748/wjg.v30.i18.2391
Published online May 14, 2024. doi: 10.3748/wjg.v30.i18.2391
Angiotensin-converting enzyme 2 and AMPK/mTOR pathway in the treatment of liver fibrosis: Should we consider further implications?
Michele Barone, Section of Gastroenterology, Department of Precision and Regenerative Medicine - Jonian Area- University of Bari, Bari 70124, Italy
Author contributions: I declare that I conceived and wrote the manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Michele Barone, MD, PhD, Associate Professor, Section of Gastro
Received: February 2, 2024
Revised: March 9, 2024
Accepted: April 17, 2024
Published online: May 14, 2024
Processing time: 98 Days and 11.5 Hours
Revised: March 9, 2024
Accepted: April 17, 2024
Published online: May 14, 2024
Processing time: 98 Days and 11.5 Hours
Core Tip
Core Tip: In the light of clarifying the link between liver fibrosis and the development of hepatocellular carcinoma, we discussed the renin-angiotensin system involvement in liver fibrosis and hepatocarcinoma development, the specific mechanisms by which angiotensin-converting enzyme 2 (ACE2) regulates hepatic stellate cell (HSC) autophagy and consequently fibrosis, and the ACE2-dependent upstream signals modulating the AMP-activated protein kinase/mammalian target of the rapamycin pathway implicated in the regulation of HSC activation.