ArticleCell death discovery2025
Astrocyte-derived CXCL10 exacerbates endothelial cells pyroptosis and blood-brain barrier disruption via CXCR3/cGAS/AIM2 pathway after intracerebral hemorrhage.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Fumarate Hydratase Lactylation Exacerbates Traumatic Brain Injury Pathology via Mitochondrial Dysfunction and Neuroinflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting Gasdermins for Therapeutic Interventions in Central Nervous System Injury.Neurotoxicity research · 2026Review
- Loss of SHP1 in Spinal Astrocytes Triggers T-Lymphocyte Infiltration and Nociceptive Hypersensitivity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Molecular Regulation of Pyroptosis in Alzheimer's Disease: Linking Neuroinflammation, Cell Death, and Therapeutic Targeting.Molecular neurobiology · 2026Review
- Microglia and neuroinflammation: function, heterogeneity, and crosstalk.Cellular & molecular immunology · 2026Review
- Expanding roles of cGAS-STING signaling in neuroinflammation.The Journal of clinical investigation · 2026Review
- Pyroptosis in cerebral ischemia‑reperfusion injury: Molecular mechanisms and therapeutic implications (Review).Molecular medicine reports · 2026Review
- Multi-omics analysis and experimental validation reveal the IRF7-CXCL10 axis as a master regulator of microglial PCD in ischemic stroke.Cell biology and toxicology · 2026Article
- Endothelial IRE1 signaling maintains blood-brain barrier integrity and limits neuroinflammation after traumatic brain injury.Cell death & disease · 2026Article
- Astrocytic CCL5 orchestrates CCR5-positive neuronal necroptosis in subarachnoid hemorrhage.Journal of neuroinflammation · 2026Article
- Healthy young human plasma-derived exosomes enhance neural stem cell therapy by suppressing pyroptosis via TXNIP/NLRP3 after intracerebral hemorrhage.Journal of nanobiotechnology · 2026Article
- Astrocyte-blood-brain barrier crosstalk in cerebral small vessel disease: linking barrier dysfunction to neurovascular failure.Frontiers in neurology · 2026Review
- CXCR3 Deficiency Alleviates Retinal Ganglion Cell Loss by Regulating Neuron-Astrocyte Communication in a Mouse Model of Glaucoma.Investigative ophthalmology & visual science · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracerebral hemorrhage (ICH) is a devastating disease that disrupts the blood-brain barrier (BBB), triggers inflammation, and leads to subsequent neurological deficits. Although the CXC chemokine receptor 3 (CXCR3) and its ligand CXCL10 are implicated in regulating inflammation, the specific role and mechanism of CXCR3 in ICH-induced BBB disruption remain unclear; furthermore, the involvement of the cGAS/AIM2 signaling pathway in endothelial pyroptosis after ICH needs further investigation. This study elucidates that activation of the CXCR3/CXCL10 axis exacerbates disruption of BBB integrity via the cGAS/AIM2 pathway following ICH. Utilizing a type IV collagenase-induced ICH model, we evaluated the therapeutic efficacy of the CXCR3 inhibitor AMG487. Results demonstrated that ICH induced the upregulation of CXCR3 and CXCL10, peaking at 24 h; immunofluorescence co-localization indicated CXCR3 was primarily localized to endothelial cells, while CXCL10 originated mainly from endothelial cells and astrocytes. AMG487 treatment improved neurological deficits and attenuated BBB disruption after ICH. Furthermore, exogenous CXCL10 activating CXCR3 upregulated the expression of cGAS/STING and pyroptosis-related proteins in vivo and vitro ICH models. However, inhibiting CXCR3 reversed the poor effects induced by CXCL10. Inhibition of the cGAS/AIM2 signaling pathway using A151 effectively reduced vascular endothelial pyroptosis and BBB disruption. In a co-culture model of endothelial cells and astrocytes, depleting CXCL10 downregulated the expression of cGAS, STING, AIM2, and pyroptosis-related proteins and alleviated endothelial pyroptosis. This study demonstrates that inhibition CXCR3 preserves BBB integrity and improves neurological deficits after ICH by suppressing endothelial pyroptosis via the cGAS/AIM2 signaling pathway. These findings provide novel insights into ICH pathogenesis, proposing CXCR3 as a potential target for BBB disruption and AMG487 as a promising therapeutic strategy for ICH patients.
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Registered trials
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