ArticlePsychoneuroendocrinology2020
Molecular markers of neuroendocrine function and mitochondrial biogenesis associated with early life stress.
Article in Psychoneuroendocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 3 of them syntheses that pooled it.
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Who cites it
17 citing papers in PubMed, 3 syntheses or guidelines pooled it, 34 citations in OpenAlex.
- Maternal Separation and Negative Renal Programming, Evidence of Morphofunctional Alterations in Rodent Models: Systematic Review and Meta-Analysis.International journal of molecular sciences · 2025Pooled it
- Whole blood mitochondrial copy number in clinical populations with mood disorders: A meta-analysis: Blood mitochondrial copy number and mood disorders.Psychiatry research · 2024Pooled it
- Childhood Adversities and Salivary Cortisol Responses to the Trier Social Stress Test: A Systematic Review of Studies Using the Children Trauma Questionnaire (CTQ).International journal of environmental research and public health · 2020Pooled it
- Early Adversity Imprints Multisystem Biological Aging: A Longitudinal Study of Adversity Dimensions and Aging Phenotypes Across Adolescence.Biological psychiatry global open science · 2026Article
- Psychological stress induced mitochondrial response in humans and its medial prefrontal biomarker correlates.Translational psychiatry · 2026Article
- Blood and neuronal extracellular vesicle mitochondrial disruptions in schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Early life stress, psychiatric conditions, and mitochondrial DNA copy number (mtDNAcn) in medically healthy young adults.Psychoneuroendocrinology · 2025Article
- Associations of maternal neighborhood and trauma-related stressors with mitochondrial DNA copy number and telomere length in maternal and cord blood.Scientific reports · 2025Article
- Increased Rate of Unique Mitochondrial DNA Deletion Breakpoints in Young Adults With Early-Life Stress.Biological psychiatry global open science · 2025Article
- Sex-specific fear acquisition following early life stress is linked to amygdala and hippocampal purine and glutamate metabolism.Communications biology · 2024Article
- Impact of lifetime stressor exposure on neuroenergetics in schizophrenia spectrum disorders.Schizophrenia research · 2024Article
- Examining the Biological Impacts of Parent-Child Relationship Dynamics on Preschool-Aged Children who have Experienced Adversity.Developmental psychobiology · 2024Observational
- Porcine blood cell and brain tissue energy metabolism: Effects of "early life stress".Frontiers in molecular biosciences · 2023Article
- A molecular framework for autistic experiences: Mitochondrial allostatic load as a mediator between autism and psychopathology.Frontiers in psychiatry · 2022Article
- Mitochondria and early-life adversity.Mitochondrion · 2021Article
- DNA Methylation of PGC-1α Is Associated With Elevated mtDNA Copy Number and Altered Urinary Metabolites in Autism Spectrum Disorder.Frontiers in cell and developmental biology · 2021Article
- The Role of Mitonuclear Incompatibility in Bipolar Disorder Susceptibility and Resilience Against Environmental Stressors.Frontiers in genetics · 2021Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveGlucocorticoid receptor gene (NR3C1) promoter methylation influences cellular expression of the glucocorticoid receptor and is a proposed mechanism by which early life stress impacts neuroendocrine function. Mitochondria are sensitive and responsive to neuroendocrine stress signaling through the glucocorticoid receptor, and recent evidence with this sample and others shows that mitochondrial DNA copy number (mtDNAcn) is increased in adults with a history of early stress. No prior work has examined the role of NR3C1 methylation in the association between early life stress and mtDNAcn alterations.
methodsAdult participants (n = 290) completed diagnostic interviews and questionnaires characterizing early stress and lifetime psychiatric symptoms. Medical conditions, active substance abuse, and prescription medications other than oral contraceptives were exclusionary. Subjects with a history of lifetime bipolar, obsessive-compulsive, or psychotic disorders were excluded; individuals with other forms of major psychopathology were included. Whole blood mtDNAcn was measured using qPCR; NR3C1 methylation was measured via pyrosequencing. Multiple regression and bootstrapping procedures tested NR3C1 methylation as a mediator of effects of early stress on mtDNAcn.
resultsThe positive association between early adversity and mtDNAcn (p = .02) was mediated by negative associations of early adversity with NR3C1 methylation (p = .02) and NR3C1 methylation with mtDNAcn (p < .001). The indirect effect involving early adversity, NR3C1 methylation, and mtDNAcn was significant (95 % CI [.002, .030]).
conclusionsNR3C1 methylation significantly mediates the association between early stress and mtDNAcn, suggesting that glucocorticoid receptor signaling may be a mechanistic pathway underlying mtDNAcn alterations of interest for future longitudinal work.
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