ArticleAnnals of neurology2012
Macrophages prevent hemorrhagic infarct transformation in murine stroke models.
Article in Annals of neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 3 of them syntheses that pooled it.
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
162 citing papers in PubMed, 3 syntheses or guidelines pooled it, 290 citations in OpenAlex.
- Systematic Review of the Differential Effects of TGF-β1 in Ischemic and Hemorrhagic Preclinical Stroke Models.Journal of the American Heart Association · 2025Pooled it
- The effects of splenectomy in murine models of ischemic stroke: a systematic review and meta-analysis.Journal of neuroinflammation · 2022Pooled it
- A systematic review of the research progress of non-coding RNA in neuroinflammation and immune regulation in cerebral infarction/ischemia-reperfusion injury.Frontiers in immunology · 2022Pooled it
- The Association Between PIV and Mortality in US Stroke Survivors: A NHANES 1999-2018 Retrospective Cohort Study.Health science reports · 2026Article
- Multimodal Single-Cell Transcriptomic and Chromatin Accessibility Profiling Reveals Monocyte-Derived Macrophage Dynamics Following Ischemic Stroke.International journal of molecular sciences · 2026Article
- Monocyte-derived macrophages and their roles in ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Targeted lipid nanoparticles containing IL-10 mRNA improve outcomes in experimental intracerebral hemorrhage.Journal of neuroinflammation · 2025Article
- Interleukin-1 regulates myeloid cell trafficking and cerebral blood flow following intracerebral haemorrhage.Disease models & mechanisms · 2025Article
- Microglia are prominent producers of inflammatory cytokines during the hyperacute phase of ischemic stroke.Communications biology · 2025Article
- Article
- Single-Cell Transcriptomes of Immune Cells from Multiple Compartments Redefine the Ontology of Myeloid Subtypes Post-Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- VEGF-E Attenuates Injury After Ischemic Stroke by Promoting Reparative Revascularization.The European journal of neuroscience · 2025Article
- Temporal Transcriptomic Differences in Stroke Between Diabetic and Non-Diabetic Mice.Journal of molecular neuroscience : MN · 2025Article
- MicroRNAs Associated with Parenchymal Hematoma After Endovascular Mechanical Reperfusion for Acute Ischemic Stroke in Rats.Biomedicines · 2025Article
- Infiltrating peripheral monocyte TREM-1 mediates dopaminergic neuron injury in substantia nigra of Parkinson's disease model mice.Cell death & disease · 2025Article
- Association between pan-immune inflammatory value and all-cause mortality in critically ill patients with ischemic stroke: a retrospective analysis of the MIMIC-IV database (2008-2022).Frontiers in neurology · 2025Article
- Systemic Inflammation Decreases Initial Brain Injury but Attenuates Neurite Extension and Synapse Formation during the Repair of Injured Brains.Experimental neurobiology · 2024Article
- IL-33/ST2 signaling in monocyte-derived macrophages maintains blood-brain barrier integrity and restricts infarctions early after ischemic stroke.Journal of neuroinflammation · 2024Article
- Review
- Advancing stroke recovery: unlocking the potential of cellular dynamics in stroke recovery.Cell death discovery · 2024Review
102 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveInflammation is increasingly viewed as a new therapeutic target in subacute stages of brain infarction. However, apart from causing secondary damage, inflammation could equally promote beneficial lesion remodeling and repair. Distinct subpopulations of monocytes/macrophages (MOs/MPs) may critically determine the outcome of lesion-associated inflammation.
methodsWe addressed the role of bone marrow-derived MOs/MPs in 2 different mouse models of ischemic stroke using a combined cell-specific depletion, chemokine receptor knockout, bone marrow chimeric, and pharmacological approach.
resultsStarting within 24 hours of stroke onset, immature Ly6c(hi) monocytes infiltrated into the infarct border zone and differentiated into mature Ly6c(lo) phagocytes within the lesion compartment. MO/MP infiltration was CCR2-dependent, whereas we did not obtain evidence for additional recruitment via CX3CR1. Depletion of circulating MOs/MPs or selective targeting of CCR2 in bone marrow-derived cells caused delayed clinical deterioration and hemorrhagic conversion of the infarctions. Bleeding frequently occurred around thin-walled, dilated neovessels in the infarct border zone and was accompanied by decreased expression of transforming growth factor (TGF)-β1 and collagen-4, along with diminished activation of Smad2. Injection of TGF-β1 into the lesion border zone greatly reduced infarct bleeding in MO/MP-depleted mice.
interpretationBone marrow-derived MOs/MPs recruited via CCR2 and acting via TGF-β1 are essential for maintaining integrity of the neurovascular unit following brain ischemia. Future therapies should be aimed at enhancing physiological repair functions of CCR2(+) MOs/MPs rather than blocking their hematogenous recruitment.
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.