Zhang YP, Liu XR, Yang MW, Yang SL, Hong FF. New progress in understanding roles of nitric oxide during hepatic ischemia-reperfusion injury. World J Hepatol 2022; 14(3): 504-515 [PMID: 35582289 DOI: 10.4254/wjh.v14.i3.504]
Corresponding Author of This Article
Fen-Fang Hong, MD, Associate Professor, Experimental Center of Pathogen Biology, College of Medicine, Nanchang University, No. 461 Bayi Road, Nanchang 330006, Jiangxi Province, China. hongfenfang@126.com
Research Domain of This Article
Pharmacology & Pharmacy
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
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: http://creativecommons.org/licenses/by-nc/4.0/
World J Hepatol. Mar 27, 2022; 14(3): 504-515 Published online Mar 27, 2022. doi: 10.4254/wjh.v14.i3.504
New progress in understanding roles of nitric oxide during hepatic ischemia-reperfusion injury
Yi-Ping Zhang, Xin-Ran Liu, Mei-Wen Yang, Shu-Long Yang, Fen-Fang Hong
Yi-Ping Zhang, Xin-Ran Liu, Fen-Fang Hong, Experimental Center of Pathogen Biology, College of Medicine, Nanchang University, Nanchang 330006, Jiangxi Province, China
Mei-Wen Yang, Department of Surgery, Fuzhou Medical College, Nanchang University, Fuzhou 344000, Jiangxi Province, China
Shu-Long Yang, Department of Physiology, College of Medicine, Nanchang University, Nanchang 330006, Jiangxi Province, China
Shu-Long Yang, Department of Physiology, Fuzhou Medical College, Nanchang University, Fuzhou 344000, Jiangxi Province, China
Author contributions: Zhang YP and Liu XR are co-first authors and contributed equally to this work, and they wrote and revised the paper; Yang MW participated in data collection and revised the paper by making point-by-point responses to the reviewers; Yang SL and Hong FF are co-corresponding authors who contributed equally to this work, and they are responsible for improving grammars and languages, conceptualizing the idea, and obtaining funding.
Conflict-of-interest statement: There is no conflict of interest associated with any of the authors or other coauthors in this manuscript.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Fen-Fang Hong, MD, Associate Professor, Experimental Center of Pathogen Biology, College of Medicine, Nanchang University, No. 461 Bayi Road, Nanchang 330006, Jiangxi Province, China. hongfenfang@126.com
Received: March 29, 2021 Peer-review started: March 29, 2021 First decision: June 15, 2021 Revised: July 9, 2021 Accepted: February 19, 2022 Article in press: February 19, 2022 Published online: March 27, 2022
Core Tip
Core Tip: This review focuses on the new progress in the understanding of the role of nitric oxide (NO) in hepatic ischemia-reperfusion injury (HIRI). NO protects HIRI by increasing NO bioavailability and cellular autophagy, down-regulating leukotriene C4 synthase, inhibiting the nuclear factor κB (NF-κB) pathway, and reducing inflammatory cytokines and reactive oxygen species. While by regulating apoptotic factors, it has dual effects. eNOS exerts hepatoprotective effects by promoting NO production through the involvement of the phosphoinositide 3-kinase/Akt pathway and Kruppel-like factor 2/adenosine monophosphate-activated protein kinase pathways. The function of eNOS overexpression remains controversial. iNOS-derived NO mainly deteriorates HIRI, but it may reduce damage under certain conditions. The balance of eNOS and iNOS is important for the HIRI protection.
