Evidence map›Paper›PMID 30531937›Full record

ArticleMolecular psychiatry2020

NDUFV2 pseudogene (NDUFV2P1) contributes to mitochondrial complex I deficits in schizophrenia.

Oded Bergman, Rachel Karry, Jumana Milhem, Dorit Ben-Shachar

Abstract read
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In one paragraph

Article in Molecular psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Oded BergmanLaboratory of Psychobiology, Department of Psychiatry, Rambam Health Care Campus, B. Rappaport Faculty of Medicine and Rappaport Family Institute for Research in Medical Sciences, Technion-Israel Institute of Technology, Haifa, Israel.
Rachel KarryLaboratory of Psychobiology, Department of Psychiatry, Rambam Health Care Campus, B. Rappaport Faculty of Medicine and Rappaport Family Institute for Research in Medical Sciences, Technion-Israel Institute of Technology, Haifa, Israel.
Jumana MilhemLaboratory of Psychobiology, Department of Psychiatry, Rambam Health Care Campus, B. Rappaport Faculty of Medicine and Rappaport Family Institute for Research in Medical Sciences, Technion-Israel Institute of Technology, Haifa, Israel.
Dorit Ben-ShacharLaboratory of Psychobiology, Department of Psychiatry, Rambam Health Care Campus, B. Rappaport Faculty of Medicine and Rappaport Family Institute for Research in Medical Sciences, Technion-Israel Institute of Technology, Haifa, Israel. shachar@technion.ac.il.
Technion – Israel Institute of Technology · ILRambam Health Care Campus · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria together with other cellular components maintain a constant crosstalk, modulating transcriptional and posttranslational processes. We and others demonstrated mitochondrial multifaceted dysfunction in schizophrenia, with aberrant complex I (CoI) as a major cause. Here we show deficits in CoI activity and homeostasis in schizophrenia-derived cell lines. Focusing on a core CoI subunit, NDUFV2, one of the most severely affected subunits in schizophrenia, we observed reduced protein level and functioning, with no change in mRNA transcripts. We further show that NDUFV2 pseudogene (NDUFV2P1) expression is increased in schizophrenia-derived cells and in postmortem brain specimens. In schizophrenia and controls pooled samples, NDUFV2P1 level demonstrated a significant inverse correlation with NDUFV2 pre- and matured protein level and with CoI-driven cellular respiration. Our data suggest a role for a pseudogene in its parent-gene regulation and possibly in CoI dysfunction in schizophrenia. The abnormal expression of the pseudogene may be one element of a vicious circle in which CoI deficits lead to mitochondrial dysfunction potentially affecting genome-wide regulation of gene expression, including the expression of pseudogenes.

Indexed as

Electron Transport Complex IGene ExpressionHumansMitochondriaNADH DehydrogenasePseudogenesRNA, MessengerSchizophreniaElectron Transport Complex INADH DehydrogenaseNDUFV2 protein, humanRNA, Messenger

Identifiers

PMID30531937
OpenAlexW2903740536

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.