ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Neutrophil Mobilization Triggers Microglial Functional Change to Exacerbate Cerebral Ischemia-Reperfusion Injury.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed.
- An integrated investigation of systemic and localized pathophysiological mechanisms of stroke and multimodal therapeutic strategies.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Association of Inflammatory Markers With Symptomatic Intracranial Hemorrhage, Malignant Cerebral Edema, and Poor Functional Recovery in Patients With Acute Ischemic Stroke Undergoing Endovascular Thrombectomy.Journal of the American Heart Association · 2026Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- GPNMB modulates neutrophil extracellular trap formation: therapeutic implications for ischemic stroke.Journal of neuroinflammation · 2026Article
- Polydatin Inhibits Neuroinflammation in Cerebral Ischemia-Reperfusion Injury Through Suppressing the CXCL3/CXCR2 Axis.CNS neuroscience & therapeutics · 2026Article
- Responsive nanoparticles modulating microglia lactate transport alleviate M1-type polarization and neuroinflammation for brain injury therapy.Journal of nanobiotechnology · 2026Article
- Dynamics of neutrophilia at the neurovascular unit arising from repeated pulmonary inflammation.Journal of neuroinflammation · 2026Article
- Flipping the Switch: MeCP2-Mediated Lactylation Rewires Microglial Metabolism and Inflammation via the HK2/mTOR Axis in Poststroke Neuroinflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The S100A8/A9-NETosis feedback loop in sepsis: potential mechanisms, immune crosstalk, and therapeutic targeting.Frontiers in immunology · 2026Review
- Neutrophils and neutrophil extracellular traps in ischaemia-reperfusion injury: pathophysiological roles and therapeutic potential.Burns & trauma · 2026Review
- Investigating the Cytoprotective Mechanisms of the Tardigrade Damage Suppressor (Dsup) Protein in Human Cells Under Hypoxic Stress.International journal of molecular sciences · 2025Article
- Dynamics of Neutrophilia at the Neurovascular Unit Arising from Repeated Pulmonary Inflammation.bioRxiv : the preprint server for biology · 2025Article
- Neutrophil Mobilization Triggers Microglial Functional Change to Exacerbate Cerebral Ischemia-Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The glia-neutrophil axis: an understudied crosstalk in bacteria-induced neuroinflammation.Frontiers in neurologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Acute ischemic stroke is a leading cause of mortality and disability worldwide. Neuroinflammation following ischemia-reperfusion plays a critical role in the disease's pathogenesis. Neutrophil aggregation and clearance within the brain parenchyma influence neuroinflammatory damage during ischemic stroke. Microglia-mediated phagocytosis plays a pivotal role in mitigating neuroinflammation and promoting brain parenchyma recovery. However, the mechanisms underlying the cross-talk between neutrophils and microglia remain poorly understood. Here, this study demonstrates that neutrophils can trigger microglial functional change to inhibit microglial phagocytosis and promote pyroptosis, which is regulated by neutrophil-derived myeloid-related protein 14. Additionally, interleukin-1β released by pyroptotic microglia further upregulates myeloid-related protein 14 expression and facilitates neutrophil mobilization from the bone marrow, establishing a self-sustaining inflammatory loop. Therefore, neutrophils accumulate in the brain parenchyma and further exacerbate microglial neuroinflammation in the ischemic brain. These findings reveal a previously unknown interaction between neutrophils and microglia after acute ischemic stroke and suggest that targeting myeloid-related protein 14 may provide a novel therapeutic strategy for ischemic stroke therapy.
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What Socratic holds
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 Socratic graph.