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. 2021 Nov 19;11(11):1075–1094. doi: 10.5498/wjp.v11.i11.1075

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©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.

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/

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The proposed signaling pathways for ERVWE1 contributes to mitochondrial energy metabolism deficiency in schizophrenia. 1: ERVWE1 suppressed cytoplasmic polyadenylation element-binding protein 1 (CPEB1) mRNA and protein expression by regulating its promoter activity; 2: ERVWE1 upregulated the expression of NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2) pseudogene (NDUFV2P1) through enhancing its promoter activity. CPEB1 downregulated NDUFV2P1 expression and functioned as a mediator of NDUFV2P1 transcript induced by ERVWE1; 3: NDUFV2P1 reduced NDUFV2 expression through inhibiting its promoter activation. Additionally, ERVWE1 decreased the mRNA and protein expression of NDUFV2 and suppressed NDUFV2 promoter through increasing NDUFV2P1 transcript. Moreover, CPEB1 was involved in regulating NDUFV2P1/NDUFV2 signaling pathway triggered by ERVWE1; 4: ERVWE1 reduced complex I activity via regulating NDUFV2 and its retrocopies expression. Decreased CPEB1 was involved in the complex I activity deficiency induced by ERVWE1; 5: Deficient complex I activity might result in mitochondrial metabolic dysregulation and contributed to the development of schizophrenia.