ArticleFrontiers in psychiatry2019
Mitochondrial Dysfunction Is Inducible in Lymphoblastoid Cell Lines From Children With Autism and May Involve the TORC1 Pathway.
Article in Frontiers in psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- A Mitochondrial Supplement Improves Function and Mitochondrial Activity in Autism: A Double-Blind Placebo-Controlled Cross-Over Trial.International journal of molecular sciences · 2025Trial
- Mitochondrial Dysfunction in Autism and Attention-Deficit/Hyperactivity Disorder: Evidence from Genetic, Biochemical, and Neuroimaging Approaches.Antioxidants (Basel, Switzerland) · 2026Review
- Transcriptomic Signatures of Mitochondrial Dysfunction in Autism: Integrated mRNA and microRNA Profiling.Genes · 2025Article
- Bioenergetic signatures of neurodevelopmental regression.Frontiers in physiology · 2024Article
- Treatment of Autism Spectrum Disorders by Mitochondrial-targeted Drug: Future of Neurological Diseases Therapeutics.Current neuropharmacology · 2023Review
- Investigating the Impact of a Curse: Diseases, Population Isolation, Evolution and the Mother's Curse.Genes · 2022Review
- Air Pollution and Maximum Temperature Are Associated with Neurodevelopmental Regressive Events in Autism Spectrum Disorder.Journal of personalized medicine · 2022Article
- Association of NGF and Mitochondrial Respiration with Autism Spectrum Disorder.International journal of molecular sciences · 2022Article
- Modern Biomarkers for Autism Spectrum Disorder: Future Directions.Molecular diagnosis & therapy · 2022Article
- A Combined Proteomics and Metabolomics Profiling to Investigate the Genetic Heterogeneity of Autistic Children.Molecular neurobiology · 2022Article
- Integrated microRNA-mRNA Expression Profiling Identifies Novel Targets and Networks Associated with Autism.Journal of personalized medicine · 2022Article
- Re-emerging concepts of immune dysregulation in autism spectrum disorders.Frontiers in psychiatry · 2022Review
- Time dependent changes in the bioenergetics of peripheral blood mononuclear cells: processing time, collection tubes and cryopreservation effects.American journal of translational research · 2022Article
- Mitochondrial morphology is associated with respiratory chain uncoupling in autism spectrum disorder.Translational psychiatry · 2021Article
- SLC25A24 gene methylation and gray matter volume in females with and without conduct disorder: an exploratory epigenetic neuroimaging study.Translational psychiatry · 2021Article
- Prenatal air pollution influences neurodevelopment and behavior in autism spectrum disorder by modulating mitochondrial physiology.Molecular psychiatry · 2021Article
- Mitochondria May Mediate Prenatal Environmental Influences in Autism Spectrum Disorder.Journal of personalized medicine · 2021Review
- An mtDNA mutant mouse demonstrates that mitochondrial deficiency can result in autism endophenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Role of Mitonuclear Incompatibility in Bipolar Disorder Susceptibility and Resilience Against Environmental Stressors.Frontiers in genetics · 2021Review
- Early life metal exposure dysregulates cellular bioenergetics in children with regressive autism spectrum disorder.Translational psychiatry · 2020Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously developed a lymphoblastoid cell line (LCL) model of mitochondrial dysfunction in autism spectrum disorder (ASD); some individuals with ASD showed mitochondrial dysfunction (AD-A) while other individuals (AD-N) demonstrated mitochondrial respiration similar to controls (CNT). To test the hypothesis that mitochondrial dysfunction could be a consequence of environmental exposures through chronic elevations in reactive oxygen species (ROS), we exposed LCLs to prolonged ROS. We also examined expression of metabolic regulatory genes and the modulating effect of the mechanistic target of rapamycin (mTOR) pathway. Prolonged ROS exposure induced or worsened mitochondrial dysfunction in all LCL groups. Expression of genes associated with ROS protection was elevated in both AD-N and AD-A LCLs, but mitochondrial fission/fusion and mitoplasticity gene expression was only increased in AD-N LCLs. Partial least squares discriminant analysis showed that mTOR, UCP2 (uncoupling protein 2), SIRT1 (sirtuin 1), and MFN2 (mitofusin-2) gene expression differentiated LCL groups. Low-dose rapamycin (0.1 nM) normalized respiration with the magnitude of this normalization greater for AD-A LCLs, suggesting that the mammalian target of rapamycin complex 1 (mTORC1) pathway may have a different dynamic range for regulating mitochondrial activity in individuals with ASD with and without mitochondrial dysfunction, potentially related to S6K1 (S6 kinase beta-1) regulation. Understanding pathways that underlie mitochondrial dysfunction in ASD may lead to novel treatments.
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