ReviewJournal of neuroinflammation2013
Leukocyte infiltration in experimental stroke.
Review in Journal of neuroinflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
96 citing papers in PubMed, 163 citations in OpenAlex.
- The kallikrein-kinin system modulates CD4Journal of neuroinflammation · 2026Article
- Colchicine as an Adjunctive Therapy to Improve Ischemic Stroke Reperfusion Outcomes in Mice.CNS neuroscience & therapeutics · 2026Article
- Systemic Inflammation and Central Neuronal Damage: The Relationship Between Neutrophil-to-Lymphocyte Ratio and Neuron-Specific Enolase in Acute Ischemic Stroke.Immunity, inflammation and disease · 2026Article
- Decoding IFN-mediated immunity and cell dynamics in viral encephalitis: Insights from coxsackievirus B3 infection.iScience · 2026Article
- Chronic Ketosis Provides Neuroprotection Through HIF- 1α-Mediated Control of the TXNIP/NLRP3 Axis by Regulating the Inflammatory and Apoptotic Response.Molecular neurobiology · 2025Article
- Mapping of blood flow and slow speckle tissue dynamics using laser speckle contrast imaging.Biomedical optics express · 2025Article
- Macrophage-mimetic liposomes co-delivering ceria and Ac2-26 peptide for penumbra protection in ischemic stroke.Journal of nanobiotechnology · 2025Article
- Review
- Neuroinflammation and acute ischemic stroke: impact on translational research and clinical care.Frontiers in surgery · 2025Review
- Circulating CD4+, CD8+, and double-negative T cells in ischemic stroke and stroke-associated infection: a prospective case-control study.Frontiers in cellular neuroscience · 2025Article
- Article
- Activation of Inflammasomes and Relevant Modulators for the Treatment of Microglia-mediated Neuroinflammation in Ischemic Stroke.Molecular neurobiology · 2024Review
- Novel Programmed Death Ligand 1-AKT-engineered Mesenchymal Stem Cells Promote Neuroplasticity to Target Stroke Therapy.Molecular neurobiology · 2024Article
- Targeting lipid nanoparticles to the blood-brain barrier to ameliorate acute ischemic stroke.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Advanced Nano-Drug Delivery Systems in the Treatment of Ischemic Stroke.Molecules (Basel, Switzerland) · 2024Review
- Mechanisms of inflammation after ischemic stroke in brain-peripheral crosstalk.Frontiers in molecular neuroscience · 2024Review
- Infiltrating myeloid cell-derived properdin markedly promotes microglia-mediated neuroinflammation after ischemic stroke.Journal of neuroinflammation · 2023Article
- Transcriptome-Wide Analysis of Neutrophil-Related Circ_22232 in Neuroinflammation from Ischemic Stroke Mice.Brain sciences · 2023Article
- Research Progress of Neutrophil-Mediated Drug Delivery Strategies for Inflammation-Related Disease.Pharmaceutics · 2023Review
- Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stroke is one of the leading causes of death worldwide. At present, the only available treatment is thrombolysis, which should be initiated no later than 4.5 hours after onset of symptoms. Several studies have shown that an attenuation of the inflammatory response in relation to stroke could widen the therapeutic window. However, the immune system has important functions following infarction, such as removal of dead cells and the subsequent astrocytosis as well as prevention of post-ischemic infection. Hence, detailed knowledge concerning the temporal profile of leukocyte infiltration is necessary in order to develop new and effective treatments.The purpose of this review is to determine the temporal profile of leukocyte (neutrophil granulocytes, macrophages and T-cells) infiltration following experimental stroke. We found that the number of neutrophil granulocytes peaks between day 1 and 3 after experimental stroke, with short occlusion times (30 and 60 minutes of middle cerebral artery occlusion (MCAO)) leading to a later peak in response (P <0.001). Macrophages/microglia were found to peak later than day 3 and stay in the infarcted area for longer time periods, whereas duration of occlusion had no influence on the temporal infiltration (P = 0.475). Studies on T-cell infiltration are few; however, a tendency towards infiltration peak at later time points (from day 4 onwards) was seen.This review provides a framework for the instigation of post-stroke anti-inflammatory treatment, which could prove beneficial and widen the therapeutic window compared to current treatment options.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.