ArticleJournal of neurochemistry2013
Insulin-like growth factor-1 abrogates microglial oxidative stress and TNF-α responses to spreading depression.
Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 4 of them syntheses that pooled it.
What it found
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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.
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Who cites it
57 citing papers in PubMed, 4 syntheses or guidelines pooled it, 96 citations in OpenAlex.
- Compartment-specific redox modulation in migraine with aura: a systematic review of context-dependent mechanisms.Journal of oral & facial pain and headache · 2026Pooled it
- Association between oxidative stress-related IGF-1 and prognosis after ischemic stroke: a systematic review and meta-analysis.Frontiers in neurology · 2025Pooled it
- Imaging the inflammatory phenotype in migraine.The journal of headache and pain · 2022Pooled it
- Effects of psychotropic drugs on inflammation: consequence or mediator of therapeutic effects in psychiatric treatment?Psychopharmacology · 2016Pooled it
- Plasma SuPAR and therapeutic response to erenumab in migraine: a REFORM study.The journal of headache and pain · 2025Trial
- Microglia maintain retinal redox homeostasis following ablation of rod photoreceptors in zebrafish.The Journal of biological chemistry · 2026Article
- Oxidative Stress in Migraine-Effect or Cause?Genes · 2026Review
- Serum tumor necrosis factor-α levels in migraine: a registry for migraine (REFORM) study.Pain reports · 2026Article
- Dietary Modulation of Migraine: Metabolic, Neuroinflammatory and Microbiota-Mediated Mechanisms.Journal of clinical medicine · 2026Review
- Intracisternal IGF-1 gene delivery attenuates early anxiety-like behavior but not dopaminergic neurodegeneration in a 6-OHDA rat model of parkinsonism.Frontiers in aging neuroscience · 2026Article
- The link between spreading depolarization and innate immunity in the central nervous system.The journal of headache and pain · 2025Review
- Association of plasma soluble urokinase plasminogen activator receptor concentrations and migraine with aura: a REFORM study.Brain communications · 2025Article
- Ginsenoside Rg1: A Neuroprotective Natural Dammarane-Type Triterpenoid Saponin With Anti-Depressive Properties.CNS neuroscience & therapeutics · 2024Review
- Identification of Bioactive Substances Derived from the Probiotic-Induced Bioconversion ofMicroorganisms · 2024Article
- A comprehensive exploration of astrocytes in migraine: a bibliometric and visual analysis.European journal of medical research · 2024Review
- Menopause-Associated Depression: Impact of Oxidative Stress and Neuroinflammation on the Central Nervous System-A Review.Biomedicines · 2024Review
- Vesicular HMGB1 release from neurons stressed with spreading depolarization enables confined inflammatory signaling to astrocytes.Journal of neuroinflammation · 2023Article
- Repositioning of Anti-Diabetic Drugs against Dementia: Insight from Molecular Perspectives to Clinical Trials.International journal of molecular sciences · 2023Review
- Cortical Spreading Depolarization and Delayed Cerebral Ischemia; Rethinking Secondary Neurological Injury in Subarachnoid Hemorrhage.International journal of molecular sciences · 2023Review
- Relationship between insulin-like growth factor-1 and cerebral small vessel disease and its mechanisms: advances in the field.Frontiers in aging neuroscience · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Spreading depression (SD), the most likely cause of migraine aura and perhaps migraine, occurs with increased oxidative stress (OS). SD increases reactive oxygen species (ROS), and ROS, in turn, can signal to increase neuronal excitability,which includes increased SD susceptibility. SD also elevates tumor necrosis factor-α (TNF-α), which increases neuronal excitability. Accordingly, we probed for the cellular origin of OS from SD and its relationship to TNF-α, which might promote SD, using rat hippocampal slice cultures. We observed significantly increased OS from SD in astrocytes and microglia but not in neurons or oligodendrocytes. Since insulin-like growth factor-1 (IGF-1) mitigates OS from SD, we determined the cell types responsible for this effect. We found that IGF-1 significantly decreased microglial but not astrocytic OS from SD. We also show that IGF-1 abrogated the SD-induced TNF-α increase. Furthermore, TNF-α application increased microglial but not astrocytic OS, an effect abrogated by IGF-1. Next,we showed that SD increased SD susceptibility, and does so via TNF-α. This work suggests that microglia promote SD via increased and interrelated ROS and TNF-α signaling. Thus, IGF-1 mitigation of microglial ROS and TNF-α responses maybe targets for novel therapeutics development to prevent SD, and perhaps migraine.
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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.