Basic Study
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World J Psychiatr. Nov 19, 2021; 11(11): 1075-1094
Published online Nov 19, 2021. doi: 10.5498/wjp.v11.i11.1075
CPEB1, a novel risk gene in recent-onset schizophrenia, contributes to mitochondrial complex I defect caused by a defective provirus ERVWE1
Ya-Ru Xia, Xiao-Cui Wei, Wen-Shi Li, Qiu-Jin Yan, Xiu-Lin Wu, Wei Yao, Xu-Hang Li, Fan Zhu
Ya-Ru Xia, Xiao-Cui Wei, Wen-Shi Li, Qiu-Jin Yan, Xiu-Lin Wu, Wei Yao, Xu-Hang Li, Fan Zhu, State Key Laboratory of Virology and Hubei Province Key Laboratory of Allergy & Immunology, Department of Medical Microbiology, School of Medicine, Wuhan University, Wuhan 430071, Hubei Province, China
Author contributions: Xia YR designed and performed the experiments and wrote the manuscript; Yan QJ and Wu XL contributed to data collection; Yao W and Li XH performed some of the cytological experiments; Li WS and Wei XC conducted the data analyses; Zhu F served on the scientific advisory board for the School of Medicine, Wuhan University, conceived the study, was in charge of the overall direction and planning, drafted the manuscript, and the paid bills for this procedure.
Supported by the National Natural Science Foundation of China, No. 81971943, No. 81772196, No. 31470264, No. 81271820, No. 30870789, and No. 30300117; the Stanley Foundation of United States, No. 06R-1366 (for Zhu F); and the Medical Science Advancement Program (Basic Medical Sciences) of Wuhan University, No. TFJC 2018002.
Institutional review board statement: The protocol of this study was approved by the Institutional Review Board of Wuhan University, School of Basic Medical Sciences, and the study was carried out in accordance with The Code of Ethics of the World Medical Association (Declaration of Helsinki) for experiments involving humans. Informed consent was obtained for experimentation with human subjects and their privacy rights were always observed.
Conflict-of-interest statement: No potential conflicts of interest.
Data sharing statement: The data used and analyzed during the current study are available from the corresponding author upon request.
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: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Fan Zhu, PhD, Director, Doctor, Professor, State Key Laboratory of Virology and Hubei Province Key Laboratory of Allergy & Immunology, Department of Medical Microbiology, School of Medicine, Wuhan University, No. 185 Donghu Road, Wuhan 430071, Hubei Province, China. fanzhu@whu.edu.cn
Received: April 25, 2021
Peer-review started: April 25, 2021
First decision: July 14, 2021
Revised: July 26, 2021
Accepted: August 25, 2021
Article in press: August 25, 2021
Published online: November 19, 2021
Processing time: 205 Days and 10.4 Hours
Core Tip

Core Tip: Schizophrenia is a devastating psychiatric disorder. Clinical studies suggest complex I deficits and abnormal expression of ERVWE1 in schizophrenia. We found that CPEB1 might be a novel blood-based biomarker for schizophrenia. Analyses indicated that ERVWE1 was negatively correlated with CPEB1 and NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2) in schizophrenia patients. CPEB1 functioned as a mediator of the NDUFV2 pseudogene (NDUFV2P1)/NDUFV2 pathway induced by ERVWE1. Moreover, ERVWE1 inhibited complex I activity via the CPEB1/NDUFV2P1/NDUFV2 pathway. Thus, CPEB1 and NDUFV2 may be independent risk factors for schizophrenia. Our findings also reveal the role of ERVWE1 in modulating mitochondrial energy metabolism in schizophrenia.