Pathogenic role of NDUFA13 inactivation in spontaneous hepatitis in mice and the mechanism.
10.12122/j.issn.1673-4254.2021.01.07
- Author:
Xiaohui XU
1
;
Rui LI
1
;
Xin ZENG
1
;
Xin WANG
1
;
Bingqian XUE
1
;
Daochao HUANG
1
;
Yi HUANG
1
Author Information
1. Institute of Pediatrics, Children's Hospital of Chongqing Medical University, Chongqing Key Laboratory of Child Infection and Immunity// Key Laboratory of Child Development and Disorders of Ministry of Education//National Clinical Research Center for Child Health and Disorders//China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing 400014, China.
- Publication Type:Journal Article
- Keywords:
NDUFA13;
NLRP3;
gene knockout mice model;
spontaneous hepatitis
- MeSH:
Animals;
Hepatitis;
Inflammasomes;
Mice;
NF-kappa B/metabolism*;
NLR Family, Pyrin Domain-Containing 3 Protein/genetics*;
Signal Transduction
- From:
Journal of Southern Medical University
2021;41(1):55-63
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the role of NDUFA13 inactivation in the pathogenesis of spontaneous hepatitis in mice and explore the possible mechanisms.
METHODS:Hepatocyte-specific NDUFA13 knockout (NDUFA13
RESULTS:Liver-specific NDUFA13 heterozygous knockout mice were successfully constructed as verified by PCR results. HE staining revealed severe liver damage in both 4- week-old and 2-year-old NDUFA13
CONCLUSIONS:Hepatocytes-specific NDUFA13 ablation can trigger spontaneous hepatitis in mice possibly mediated by the activation of ROS/NF-κB/NLRP3 signaling.
