ArticleCNS neuroscience & therapeutics2021
AIM2 deletion enhances blood-brain barrier integrity in experimental ischemic stroke.
Article in CNS neuroscience & therapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 73 citations in OpenAlex.
- Serum AIM2 as a Prognostic Biomarker for Disease Severity and Delirium in Acute Pancreatitis: A Multicenter Prospective Cohort Study.Brain and behavior · 2026Article
- CRISPR-Based Gene Therapy for Brain Disease.Molecular neurobiology · 2026Review
- The Upregulation of AIM2 in the Central Nucleus of the Amygdala Correlates with Pain Induced by Tooth Movement.International journal of molecular sciences · 2026Article
- CRISPR-Based Therapy for Ischemic Stroke: A Narrative Review.Cellular and molecular neurobiology · 2026Review
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- Acupuncture in Cerebral Ischemia-Reperfusion Injury: A Mechanistic Narrative Review of Innate Immune Sensing and Regulated Cell Death-Related Inflammatory Amplification.International journal of general medicine · 2026Review
- Mollugin attenuates oxygen-glucose deprivation/reperfusion-induced brain microvascular endothelial cell death and permeability through activation of BDNF/TrkB-modulated Akt pathway.Journal of bioenergetics and biomembranes · 2025Article
- Immunological Mechanisms and Therapeutic Strategies in Cerebral Ischemia-Reperfusion Injury: From Inflammatory Response to Neurorepair.International journal of molecular sciences · 2025Review
- Tirzepatide mitigates Stroke-Induced Blood-Brain barrier disruption by modulating Claudin-1 and C/EBP-α pathways.Molecular medicine (Cambridge, Mass.) · 2025Article
- ALDH2 Attenuates Blood-Brain Barrier Injury Induced by Cerebral Ischemia/Reperfusion via Alleviating ROS/NLRP3 Inflammasome Axis.Neurochemical research · 2025Article
- Targeting PD-L1 for Ischemic Stroke Recovery: Age-Dependent Modulation of Immune and BBB Pathways.CNS neuroscience & therapeutics · 2025Article
- 3-HKA Promotes Vascular Remodeling After Stroke by Modulating the Activation of A1/A2 Reactive Astrocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeting inflammasome pathway towards therapeutics of neurodegenerative diseases.Organelle (Tucson, Ariz.) · 2025Article
- Activation of Inflammasomes and Relevant Modulators for the Treatment of Microglia-mediated Neuroinflammation in Ischemic Stroke.Molecular neurobiology · 2024Review
- Conditional knockout of AIM2 in microglia ameliorates synaptic plasticity and spatial memory deficits in a mouse model of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Article
- Article
- Interleukin-22 Contributes to Blood-Brain Barrier Disruption via STAT3/VEGFA Activation inACS infectious diseases · 2024Article
- Inflammasomes in neurological disorders - mechanisms and therapeutic potential.Nature reviews. Neurology · 2024Review
- SRGN amplifies microglia-mediated neuroinflammation and exacerbates ischemic brain injury.Journal of neuroinflammation · 2024Article
- The role of AIM2 in inflammation and tumors.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
aimsIschemic stroke is a life-threatening disease with limited therapeutic strategies. Blood-brain barrier (BBB) disruption is a critical pathological process that contributes to poor outcomes in ischemic stroke. We previously showed that the microglial inhibition of the inflammasome sensor absent in melanoma 2 (AIM2) suppressed the inflammatory response and protected against ischemic stroke. However, whether AIM2 is involved in BBB disruption during cerebral ischemia is unknown.
methodsMiddle cerebral artery occlusion (MCAO) and oxygen-glucose deprivation/reoxygenation (OGD/R) were used to mimic cerebral ischemia in mice and brain microvascular endothelial cells (HBMECs), respectively. The infarct volume, neurological deficits, and BBB permeability were measured in mice after MCAO. Transendothelial electrical resistance (TEER) and neutrophil adhesion to the HBMEC monolayer were assessed after OGD/R treatment. Western blot and immunofluorescence analyses were conducted to evaluate the expression of related proteins.
resultsAIM2 was shown to be expressed in brain endothelial cells and upregulated after ischemic stroke in the mouse brain. AIM2 deletion reduced the infarct volume, improved neurological and motor functions, and decreased BBB disruption. In vitro, OGD/R significantly increased the protein levels of AIM2 and ICAM-1 and decreased those of the tight junction (TJ) proteins ZO-1 and occludin. AIM2 knockdown effectively protected BBB integrity by promoting the expression of TJ proteins and decreasing ICAM-1 expression and neutrophil adhesion. Mechanistically, AIM2 knockdown reversed the OGD/R-induced increases in ICAM-1 expression and STAT3 phosphorylation in brain endothelial cells. Furthermore, treatment with the p-STAT3 inhibitor AG490 mitigated the effect of AIM2 on BBB breakdown.
conclusionOur findings indicated that inhibiting AIM2 preserved the BBB integrity after ischemic stroke, at least partially by modulating STAT3 activation and that AIM2 may be a promising therapeutic target for cerebral ischemic stroke.
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