ReviewPediatrics2014
Deficits in bioenergetics and impaired immune response in granulocytes from children with autism.
Review in Pediatrics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled 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.
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
68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 118 citations in OpenAlex.
- Nrf2 Activators as Dietary Phytochemicals Against Oxidative Stress, Inflammation, and Mitochondrial Dysfunction in Autism Spectrum Disorders: A Systematic Review.Frontiers in psychiatry · 2020Pooled it
- Pooled it
- A Mitochondrial Supplement Improves Function and Mitochondrial Activity in Autism: A Double-Blind Placebo-Controlled Cross-Over Trial.International journal of molecular sciences · 2025Trial
- Efficacy and Safety of AltibrainCurrent pharmaceutical design · 2025Trial
- Sulforaphane treatment of autism spectrum disorder (ASD).Proceedings of the National Academy of Sciences of the United States of America · 2014Trial
- Article
- A Developmental Neuroimmune Cascade Model of Autism Spectrum Disorder.International journal of molecular sciences · 2026Review
- Redox System Dysfunction as a Key Mechanism in Autism Spectrum Disorder Pathogenesis.International journal of molecular sciences · 2025Review
- Transcriptomic Signatures of Mitochondrial Dysfunction in Autism: Integrated mRNA and microRNA Profiling.Genes · 2025Article
- Clinical and Behavioral Correlates of Blood Acylcarnitine Profiles in Children with Autism Spectrum Disorder: A Cross-Sectional Analysis.Children (Basel, Switzerland) · 2025Article
- Oxidative stress response and NRF2 signaling pathway in autism spectrum disorder.Redox biology · 2025Review
- Modulating autism spectrum disorder pathophysiology using a trace amine-focused approach: targeting the gut.Molecular medicine (Cambridge, Mass.) · 2025Review
- Crosstalk Between Mitochondrial DNA and Immune Response: Focus on Autism Spectrum Disorder.Molecular neurobiology · 2025Review
- The Role of Oxidative Stress in Autism Spectrum Disorder Pathophysiology, Diagnosis and Treatment.Biomedicines · 2025Review
- Bioenergetic and Inflammatory Alterations in Regressed and Non-Regressed Patients with Autism Spectrum Disorder.International journal of molecular sciences · 2024Article
- Bioenergetic signatures of neurodevelopmental regression.Frontiers in physiology · 2024Article
- Article
- Autistic spectrum disorder (ASD) - Gene, molecular and pathway signatures linking systemic inflammation, mitochondrial dysfunction, transsynaptic signalling, and neurodevelopment.Brain, behavior, & immunity - health · 2023Article
- Viruses and autism: A Bi-mutual cause and effect.World journal of virology · 2023Review
- Association of NEF2L2 Rs35652124 Polymorphism with Nrf2 Induction and Genotoxic Stress Biomarkers in Autism.Genes · 2023Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Despite the emerging role of mitochondria in immunity, a link between bioenergetics and the immune response in autism has not been explored. Mitochondrial outcomes and phorbol 12-myristate 13-acetate (PMA)-induced oxidative burst were evaluated in granulocytes from age-, race-, and gender-matched children with autism with severity scores of ≥7 (n = 10) and in typically developing (TD) children (n = 10). The oxidative phosphorylation capacity of granulocytes was 3-fold lower in children with autism than in TD children, with multiple deficits encompassing ≥1 Complexes. Higher oxidative stress in cells of children with autism was evidenced by higher rates of mitochondrial reactive oxygen species production (1.6-fold), higher mitochondrial DNA copy number per cell (1.5-fold), and increased deletions. Mitochondrial dysfunction in children with autism was accompanied by a lower (26% of TD children) oxidative burst by PMA-stimulated reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase and by a lower gene expression (45% of TD children's mean values) of the nuclear factor erythroid 2-related factor 2 transcription factor involved in the antioxidant response. Given that the majority of granulocytes of children with autism exhibited defects in oxidative phosphorylation, immune response, and antioxidant defense, our results support the concept that immunity and response to oxidative stress may be regulated by basic mitochondrial functions as part of an integrated metabolic network.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.