ArticleCell death & disease2019
Microglial TREM-1 receptor mediates neuroinflammatory injury via interaction with SYK in experimental ischemic stroke.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers.
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Who cites it
143 citing papers in PubMed, 292 citations in OpenAlex.
- Blood-Based Biomarkers for Post-Stroke Cognitive Impairment.Current issues in molecular biology · 2026Review
- Microglial CARD19 ameliorates post-stroke neuroinflammation by stabilizing mitochondrial cristae.Neural regeneration research · 2026Article
- Systems biology-based drug repurposing for neuroinflammation treatment in activated human microglia.Scientific reports · 2026Article
- IFI204 drives gasdermin D-mediated mitochondrial permeabilization to amplify neuronal pyroptosis in ischemic stroke.Journal of neuroinflammation · 2026Article
- HIV gp120 induces TREM1 expression through TLR-PGE₂ signalling in human monocyte-derived microglia.Journal of neuroinflammation · 2026Article
- Associations of serum sTREM-1 and sTREM-2 with mortality and neurological prognosis in patients resuscitated from cardiac arrest: a machine learning-based approach.Frontiers in medicine · 2026Article
- Infralimbic Cortex Microglial TREM-1 Mediates Neuroinflammation and Exacerbates Depressive-Like Behaviors in Parkinson's Disease Model Mice.Inflammation · 2025Article
- Interaction Between Microglial Lipid Droplet Metabolism and Immune Polarisation After Stroke: Mechanisms and Therapeutic Prospects.Cellular and molecular neurobiology · 2025Review
- Review
- Lipid metabolism in microglia: Emerging mechanisms and therapeutic opportunities for neurodegenerative diseases (Review).International journal of molecular medicine · 2025Review
- hUMSC-Exosomes suppress TREM1-p38 MAPK signaling via HMGB1-dependent mechanisms to reprogram microglial function and promote neuroprotection in ischemic stroke.Journal of nanobiotechnology · 2025Article
- Contralateral Structure and Molecular Response to Severe Unilateral Brain Injury.Brain sciences · 2025Article
- TREM2-mediated regulation of microglial activity: a promising target for the treatment of ischemic stroke.Journal of translational medicine · 2025Review
- IFI204 in microglia mediates traumatic brain injury-induced mitochondrial dysfunction and pyroptosis via SENP7 interaction.Cell biology and toxicology · 2025Article
- Sulfasalazine improves neuronal function in mice with ischemic stroke by inhibiting the STING/NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Transcriptomics, single-cell sequencing and spatial sequencing-based studies of cerebral ischemia.European journal of medical research · 2025Review
- Gut-derived macrophages link intestinal damage to brain injury after cardiac arrest through TREM1 signaling.Cellular & molecular immunology · 2025Article
- Role of triggering receptor expressed on myeloid cells 1/2 in secondary injury after cerebral hemorrhage.World journal of clinical cases · 2025Review
- Combined Analysis of Human and Experimental Rat Samples Identified Biomarkers for Ischemic Stroke.Molecular neurobiology · 2025Article
- The properties of TREM1 and its emerging role in pain-related diseases.Molecular brain · 2025Review
83 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammation is initiated in response to ischemic stroke, generally with the hallmarks of microglial activation and collateral brain injury contributed by robust inflammatory effects. Triggering receptor expressed on myeloid cells (TREM)-1, an amplifier of the innate immune response, is a critical regulator of inflammation. This study identified that microglial TREM-1 expression was upregulated following cerebral ischemic injury. After pharmacologic inhibition of TREM-1 with synthetic peptide LP17, ischemia-induced infarction and neuronal injury were substantially alleviated. Moreover, blockade of TREM-1 can potentiate cellular proliferation and synaptic plasticity in hippocampus, resulting in long-term functional improvement. Microglial M1 polarization and neutrophil recruitment were remarkably abrogated as mRNA levels of M1 markers, chemokines, and protein levels of myeloperoxidase and intracellular adhesion molecule-1 (ICAM-1) were decreased by LP17. Mechanistically, both in vivo and in vitro, we delineated that TREM-1 can activate downstream pro-inflammatory pathways, CARD9/NF-κB, and NLRP3/caspase-1, through interacting with spleen tyrosine kinase (SYK). In addition, TREM-1-induced SYK initiation was responsible for microglial pyroptosis by elevating levels of gasdermin D (GSDMD), N-terminal fragment of GSDMD (GSDMD-N), and forming GSDMD pores, which can facilitate the release of intracellular inflammatory factors, in microglia. In summary, microglial TREM-1 receptor yielded post-stroke neuroinflammatory damage via associating with SYK.
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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.