ReviewInternational journal of molecular sciences2025
Mitochondrial Oxidative Phosphorylation System Dysfunction in Schizophrenia.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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.
Who cites it
15 citing papers in PubMed.
- Aging in Schizophrenia: Clinical, Biological, and Psychosocial Perspectives.Geriatrics (Basel, Switzerland) · 2026Review
- Schizophrenia: Converging Neurobiological Mechanisms and Emerging Therapeutic Strategies.Biomolecules · 2026Review
- Ultrastructural disturbances of pericapillary microglia, perioligodendrocyte microglia, oligodendrocytes and their interactions in postmortem caudate nucleus in schizophrenia.European archives of psychiatry and clinical neuroscience · 2026Article
- Review
- Decoding shared pathogenic networks of oxidative stress in neuropsychiatric disorders to prioritize multi-target therapeutics from natural products.Cell biology and toxicology · 2026Article
- Metabolic Mechanisms in Electroconvulsive Therapy for Schizophrenia: Role, Potential and Future Directions.International journal of molecular sciences · 2026Review
- Abnormal plasma oxidative stress markers in first-episode schizophrenia and associations with clinical symptoms and cognitive function.Schizophrenia (Heidelberg, Germany) · 2026Article
- Preliminary Exploration on Melatonin-Mediated Protective Effects in Intracranial Aneurysms: Transcriptomic, Proteomic, and Metabolomic Profiling of Cerebral Vascular Tissues Combined with in vivo Animal Experiments.Drug design, development and therapy · 2026Article
- Oxidative Damage Induced Disruption of Mitochondrial Quality Control Underlying Abnormal Energy Metabolism in Peripheral Leukocytes of Schizophrenia Patients.Schizophrenia bulletin open · 2026Article
- Heterogeneity-Aware, Multiscale Annotation of Shared and Specific Neurobiological Signatures among Major Neurodevelopmental Disorders.Research (Washington, D.C.) · 2026Article
- Altered Co-Expression Patterns of Mitochondrial NADH-Dehydrogenase Genes in the Prefrontal Cortex of Rodent ADHD Models.International journal of molecular sciences · 2025Article
- Long non-coding RNA Cerox1 targets components of the mitochondrial electron transport chain to regulate the memory impairment caused by sleep deprivation.Research square · 2025Article
- Aging-Related Obesity: Unveiling Mitochondrial and Metabolic Dysfunction.Current nutrition reports · 2025Review
- The Ketogenic Diet: An Anti-Inflammatory Treatment for Schizophrenia?Journal of inflammation research · 2025Review
- Multi-omics identification and validation of oxidative phosphorylation-related hub genes in schizophrenia.Frontiers in genetics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schizophrenia (SCZ) is a severe, chronic mental disorder of unknown etiology and limited therapeutic options. Bioenergetic deficits in the oxidative phosphorylation system (OXPHOS) during early postnatal brain development may underlie disrupted neuronal metabolism and synaptic signaling, contributing to the neurodevelopmental and behavioral disturbances observed in patients. This narrative review summarizes updated evidence linking mitochondrial-OXPHOS dysfunction to SCZ pathophysiology. The novelty lies in the focus on OXPHOS dysfunction at the enzymatic/functional level, rather than on genetic, transcriptional, or oxidative parameters. While complex I impairment has long been highlighted and proposed as a peripheral marker of the disease, recent studies also report alterations in other OXPHOS complexes and their precursors. These findings suggest that OXPHOS dysfunction is not isolated to a single enzymatic component but affects broader mitochondrial function, alongside oxidative stress, contributing to disease progression through mechanisms involving apoptosis, accelerated aging, and synaptic deterioration. OXPHOS dysfunction in both central and peripheral tissues further supports its relevance to SCZ. Overall, the literature points to mitochondrial OXPHOS abnormalities as a significant biological feature of SCZ. Whether these alterations are causal factors or consequences of disease processes remains unclear. Understanding OXPHOS dysregulation may open new avenues for targeted therapies.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.