ArticleJACS Au2025
Superoxide Anion-Dependent Mitochondrial Fission Contributes to Hippocampal Synaptic Dysfunction in Stress-Susceptible Mice.
Article in JACS Au, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Systematic Screening of Depression-Related Neurotoxicity Across 26 Bisphenols Reveals an ESR1-CREB1-GRIN2B-Associated Mechanism.International journal of molecular sciences · 2026Article
- Stem Cell-Derived Extracellular Vesicles Ameliorate the Neuron Mitochondrial Damage Induced by ROS-, LPS-Exposure: In Vitro Model of Neuron, Microglia, and Astrocyte Triple Co-Culture.International journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reduced synaptic plasticity of hippocampal neurons is a core aspect of depression. Mitochondrial dysfunction affects the synaptic plasticity of neurons. However, the characteristics and molecular mechanisms of mitochondrial dysfunction in hippocampal neurons remain unclear. Oxidative stress observed in depression suggests that excess superoxide anion radical (O
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Registered trials
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