Evidence map›Paper›PMID 27412728›Full record

ReviewCanadian journal of psychiatry. Revue canadienne de psychiatrie2016

Mitochondrial Oxidative Phosphorylation System (OXPHOS) Deficits in Schizophrenia: Possible Interactions with Cellular Processes.

Oded Bergman, Dorit Ben-Shachar

Open access · bronzeAbstract readReview
In one paragraph

Review in Canadian journal of psychiatry. Revue canadienne de psychiatrie, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 3% 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

91 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.

  1. Pooled it
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  15. Evolution is in the details: Regulatory differences in modern human and Neanderthal.Computational and structural biotechnology journal · 2025
    Article
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  19. Network-based drug repurposing for schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  20. Article

31 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Oded BergmanLaboratory of Psychobiology, Department of Psychiatry, Rambam Medical Center, Technion-IIT, Haifa, Israel B. Rappaport Faculty of Medicine, Technion-IIT, Haifa, Israel.
Dorit Ben-ShacharLaboratory of Psychobiology, Department of Psychiatry, Rambam Medical Center, Technion-IIT, Haifa, Israel B. Rappaport Faculty of Medicine, Technion-IIT, Haifa, Israel shachar@tx.technion.ac.il.
Technion – Israel Institute of Technology · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are key players in the generation and regulation of cellular bioenergetics, producing the majority of adenosine triphosphate molecules by the oxidative phosphorylation system (OXPHOS). Linked to numerous signaling pathways and cellular functions, mitochondria, and OXPHOS in particular, are involved in neuronal development, connectivity, plasticity, and differentiation. Impairments in a variety of mitochondrial functions have been described in different general and psychiatric disorders, including schizophrenia (SCZ), a severe, chronic, debilitating illness that heavily affects the lives of patients and their families. This article reviews findings emphasizing the role of OXPHOS in the pathophysiology of SCZ. Evidence accumulated during the past few decades from imaging, transcriptomic, proteomic, and metabolomic studies points at OXPHOS deficit involvement in SCZ. Abnormalities have been reported in high-energy phosphates generated by the OXPHOS, in the activity of its complexes and gene expression, primarily of complex I (CoI). In addition, cellular signaling such as cAMP/protein kinase A (PKA) and Ca(+2), neuronal development, connectivity, and plasticity have been linked to OXPHOS function and are reported to be impaired in SCZ. Finally, CoI has been shown as a site of interaction for both dopamine (DA) and antipsychotic drugs, further substantiating its role in the pathology of SCZ. Understanding the role of mitochondria and the OXPHOS in particular may encourage new insights into the pathophysiology and etiology of this debilitating disorder.

Indexed as

Oxidative PhosphorylationHumansMitochondriaMitochondrial DiseasesSchizophreniaSignal TransductioncAMP/PKA and Ca+2 signalingcomplex Idopaminemitochondrianeurodevelopment and plasticityoxidative phosphorylation systemSchizophrenia

Identifiers

PMID27412728
PMCPMC4959648
OpenAlexW2465324331

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.