Guan LY, Fu PY, Li PD, Li ZN, Liu HY, Xin MG, Li W. Mechanisms of hepatic ischemia-reperfusion injury and protective effects of nitric oxide. World J Gastrointest Surg 2014; 6(7): 122-128 [PMID: 25068009 DOI: 10.4240/wjgs.v6.i7.122]
Corresponding Author of This Article
Wei Li, MD, PhD, Department of Hepatobiliary-Pancreatic Surgery, Third Hospital (China-Japan Union Hospital) of Jilin University, 126 Xiantai Street, Changchun 130033, Jilin Province, China. weili888@hotmail.com
Research Domain of This Article
Immunology
Article-Type of This Article
Review
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/
Lian-Yue Guan, Pei-Yao Fu, Pei-Dong Li, Zhuo-Nan Li, Hong-Yu Liu, Wei Li, Department of Hepatobiliary-Pancreatic Surgery, Third Hospital (China-Japan Union Hospital) of Jilin University, Changchun 130033, Jilin Province, China
Min-Gang Xin, Departments of Anesthesiology, Third Hospital (China-Japan Union Hospital) of Jilin University, Changchun 130033, Jilin Province, China
Author contributions: Guan LY and Fu PY contributed equally to the paper; Guan LY primarily drafted the article; Fu PY performed the intensive revision and drew the two figures; Li PD drafted the nitric oxide portion of the manuscript; Li ZN, Liu HY and Xin MG conducted the data collection and interpretation, selected the references, and drafted the discussion; Li W contributed to the concept design, critical revision and finalization of the manuscript.
Supported by National Natural Science Foundation of China, No. 81170416 and No. 81273264; Doctoral Fund of Ministry of Education of China, No. 20100061110069; Jilin Province Science and Technology Bureau International Cooperation Fund, No. 2011742; Techpool Research Fund, No. 01201046; Jilin Province Nature Science Foundation, No. 201015178
Correspondence to: Wei Li, MD, PhD, Department of Hepatobiliary-Pancreatic Surgery, Third Hospital (China-Japan Union Hospital) of Jilin University, 126 Xiantai Street, Changchun 130033, Jilin Province, China. weili888@hotmail.com
Telephone: +86-431-89876816 Fax: +86-431-84641026
Received: January 4, 2014 Revised: May 26, 2014 Accepted: June 20, 2014 Published online: July 27, 2014 Processing time: 201 Days and 19.9 Hours
Abstract
Hepatic ischemia-reperfusion injury (IRI) is a pathophysiological event post liver surgery or transplantation and significantly influences the prognosis of liver function. The mechanisms of IRI remain unclear, and effective methods are lacking for the prevention and therapy of IRI. Several factors/pathways have been implicated in the hepatic IRI process, including anaerobic metabolism, mitochondria, oxidative stress, intracellular calcium overload, liver Kupffer cells and neutrophils, and cytokines and chemokines. The role of nitric oxide (NO) in protecting against liver IRI has recently been reported. NO has been found to attenuate liver IRI through various mechanisms including reducing hepatocellular apoptosis, decreasing oxidative stress and leukocyte adhesion, increasing microcirculatory flow, and enhancing mitochondrial function. The purpose of this review is to provide insights into the mechanisms of liver IRI, indicating the potential protective factors/pathways that may help to improve therapeutic regimens for controlling hepatic IRI during liver surgery, and the potential therapeutic role of NO in liver IRI.
Core tip: This review provides insights into several key mechanisms of liver ischemia-reperfusion injury, including the effects of anaerobic metabolism and the role of mitochondria, oxidative stress, intracellular calcium overload, liver Kupffer cells and neutrophils, and cytokines and chemokines; and summarizes the protective effects of nitric oxide.
