Study on mechanism of NOXs in liver fibrosis
10.3969/j.issn.1001-1978.2016.11.003
- VernacularTitle:NOXs在肝纤维化中的作用机制研究
- Author:
Mianli BIAN
;
Xingran CHEN
;
Chenxi ZHANG
;
Huanhuan JIN
;
Shifeng ZHAO
;
Feng ZHANG
;
Shizhong ZHENG
- Publication Type:Journal Article
- Keywords:
liver fibrosis;
NOXs;
hepatocyte apoptosis;
inflam-mation;
oxidative stress;
endoplasmic reticulum stress;
IRE1α-XBP1 signaling pathway
- From:
Chinese Pharmacological Bulletin
2016;32(11):1490-1493
- CountryChina
- Language:Chinese
-
Abstract:
Nicotinamide adenine dinucleotide phosphate oxidase ( NOXs) contributes to the production of reactive oxygen species ( ROS) in liver fibrosis, resulting in the activation of endoplas-mic reticulum stress ( ERS ) and IRE1α-XBP1 signaling path-way. ROS is a series of oxygen metabolites and its derivatives, produced by the single electron reduction of molecular oxygen ( O2 ) , including superoxide anion ( O2- ) , hydroxyl radical (-OH) , hydrogen peroxide ( H2 O2 ) , hypochlorite ion ( OCl-) and so on. They can interact with a large number of molecules, including small inorganic molecules, proteins, lipids, carbohy-drates and nucleic acids, resulting in lipid peroxidation of cell damaging molecules. And as a second messenger, ROS can also affect the proliferation and activation of HSC in liver fibrosis, and induce the hepatocyte apoptosis through a variety of cellular signal transduction. Here we review the current status of the study on the mechanism of NOXs in liver fibrosis.
