ArticleJournal of neuroinflammation2022
Inhibition of CCR2 attenuates neuroinflammation and neuronal apoptosis after subarachnoid hemorrhage through the PI3K/Akt pathway.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 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
45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.
- Causal Relationships Between Gut Microbiota, Inflammatory Cells/Proteins, and Subarachnoid Hemorrhage: A Multi-omics Bidirectional Mendelian Randomization Study and Meta-analysis.Molecular neurobiology · 2024Pooled it
- The Role of MicroRNAs in Predicting the Neurological Outcome of Patients with Subarachnoid Hemorrhage: A Meta-analysis.Cellular and molecular neurobiology · 2023Pooled it
- Astragaloside IV Mitigates Subarachnoid Hemorrhage-Induced Brain Injury via Regulating Microglial Polarization and Neuroinflammation Mediated by cGAS/STING Pathway.Chinese journal of integrative medicine · 2026Article
- Blockade of IRE1-XBP1 Signaling Pathway Ameliorates IL-6-dependent Nerve Damage and Neuron Pyroptosis after Subarachnoid Hemorrhage in Mice.Experimental neurobiology · 2026Article
- Lactate alleviates early brain damage after subarachnoid hemorrhage: Regulation of lipid metabolism.Neural regeneration research · 2026Article
- Microglia Attenuate Neuroinflammation After Subarachnoid Hemorrhage by Modulating Astrocyte Phenotypic Transformation via the RARα/Mafb/Msr1 Pathway.Molecular neurobiology · 2026Article
- Targeting the Gpr125-Gper1 axis: a novel osteogenic signaling pathway with therapeutic potential against osteoporosis.Journal of translational medicine · 2026Article
- Maraviroc Attenuates Neuronal Apoptosis by Inhibiting CCR5-Mediated Microglial Activation After Subarachnoid Hemorrhage.Neurochemical research · 2026Article
- Laminarin attenuates neuroinflammation in MPTP-induced Parkinson's disease mouse model via inhibiting dectin-1/Syk/NF-κB signaling.Inflammopharmacology · 2026Article
- Roles of myeloperoxidase and the AMPK/PI3K/AKT/eNOS pathway in osimertinib-induced cardiotoxicity: multilevel evidence from disequilibrium analysis, network pharmacology, mendelian randomization, and animal experiments.Frontiers in pharmacology · 2026Article
- Clinical Significance of Serum CCR2 and IDO1 in Diabetic Peripheral Neuropathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Neuroinflammation and Disease: Pathways and Opportunities.Annual review of pharmacology and toxicology · 2026Review
- Early CCR2-dependent monocyte recruitment defines a critical neuroinflammatory window after subarachnoid hemorrhage.Frontiers in immunology · 2026Article
- Unlocking therapeutic potential in traumatic brain injury: exploring microenvironmental targets, signaling pathways and translational hurdles.Inflammopharmacology · 2025Review
- GPR30 Inhibits Neuronal Apoptosis After Subarachnoid Hemorrhage by Activating the Wnt/β-Catenin Pathway in a m6A-dependent Manner.Molecular neurobiology · 2025Article
- Chemokine Receptor 2 Is a Theranostic Biomarker for Abdominal Aortic Aneurysms.JACC. Basic to translational science · 2025Article
- Screening, Analysis, and Validation of Endoplasmic Reticulum Stress-Related DEGs in Epilepsy.Cellular and molecular neurobiology · 2025Article
- Anti-Inflammatory Treatment of Subarachnoid Hemorrhage by Self-Assembled Silymarin Nanoparticles.Small science · 2025Article
- Itaconate promotes mitophagy to inhibit neuronal ferroptosis after subarachnoid hemorrhage.Apoptosis : an international journal on programmed cell death · 2025Article
- PARP9 exacerbates apoptosis and neuroinflammation via the PI3K pathway in the thalamus and hippocampus and cognitive decline after cortical infarction.Journal of neuroinflammation · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNeuroinflammation and neuronal apoptosis are closely associated with a poor prognosis in patients with subarachnoid hemorrhage (SAH). We investigated the role of C-C motif chemokine receptor 2 (CCR2) in SAH.
methodsPre-processed RNA-seq transcriptome datasets GSE167110 and GSE79416 from the Gene Expression Omnibus (GEO) database were screened for genes differentially expressed between mice with SAH and control mice, using bioinformatics analysis. The endovascular perforation model was performed to establish SAH. RS504393 (a CCR2 antagonist) and LY294002 (PI3K inhibitor) were administered to explore the mechanism of neuroinflammation after SAH. SAH grading, neurological scoring, brain water content and blood-brain barrier (BBB) permeability determination, enzyme-linked immunosorbent assay (ELISA), western blotting, and immunofluorescence were performed. An in vitro model of SAH was induced in H22 cells by hemin treatment. The protective mechanism of CCR2 inhibition was studied by adding RS504393 and LY294002. Clinical cerebrospinal fluid (CST) samples were detected by ELISA.
resultsExpression of CCR2 was upregulated in both datasets and was identified as a hub gene. CCR2 expression was significantly upregulated in the cytoplasm of neurons after SAH, both in vitro and in vivo. RS significantly reduced the brain water content and blood-brain barrier permeability, alleviated neuroinflammation, and reduced neuronal apoptosis after SAH. Additionally, the protective effects of CCR2 inhibition were abolished by LY treatment. Finally, the levels of CCR2, inflammatory factors, and apoptotic factors were elevated in the CSF of patients with SAH. CCR2 levels were associated with patient outcomes at the 6-month follow-up.
conclusionCCR2 expression was upregulated in both in vitro and in vivo SAH models. Additionally, inhibition of CCR2, at least partly through the PI3K/AKT pathway, alleviated neuroinflammation and neuronal apoptosis in vivo and in vitro. CCR2 levels in the CSF have a moderate diagnostic value for 6-month outcome prediction in patients with SAH.
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.