ArticleMolecular brain2017
TREM2 protects against cerebral ischemia/reperfusion injury.
Article in Molecular brain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.
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Who cites it
83 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.
- Role and Mechanism of Microglia in White Matter Injury Recovery in Ischemic Stroke.Immunity, inflammation and disease · 2025Pooled it
- Elamipretide (SS-31) and Nicotinamide Mononucleotide (NMN) Combination Therapy Targets TREM2 to Mitigate Post-ischemic Brain Injury in Mice.Neurochemical research · 2026Article
- Lipid metabolism, microglia, and stroke.Neural regeneration research · 2026Article
- Trem2 exacerbates ischemic brain injury through Gpnmb in a photothrombotic stroke model.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- GALNT3 Inhibits the Progression of Cerebral Ischemia-Reperfusion Injury by Stabilizing TREM2 via O-GalNAc Glycosylation.CNS neuroscience & therapeutics · 2026Article
- Multi-omics reveals the protective mechanisms ofFrontiers in pharmacology · 2026Article
- Role of TREM2 in neuroinflammation regulation: mechanisms, disease associations, and therapeutic translation advances.Journal of translational medicine · 2025Review
- A Novel HNeurochemical research · 2025Article
- Soluble Triggering Receptor Expressed on Myeloid Cells 2 as a Promising Biomarker for Poststroke Depression After Acute Ischemic Stroke.Journal of the American Heart Association · 2025Article
- The role of efferocytosis in ischemic stroke and insights from retinopathy.Trends in neurosciences · 2025Review
- TREM2-mediated regulation of microglial activity: a promising target for the treatment of ischemic stroke.Journal of translational medicine · 2025Review
- TREM2 Impairs Glycolysis to Interrupt Microglial M1 Polarization and Inflammation via JAK2/STAT3 Axis.Cell biochemistry and biophysics · 2025Article
- Lipid droplets in central nervous system and functional profiles of brain cells containing lipid droplets in various diseases.Journal of neuroinflammation · 2025Review
- ADAM17 Inhibition Protects Cognition in Intermittent Hypoxia: The Role of TREM2.Nature and science of sleep · 2025Article
- Estrogen and progesterone attenuate CD4-positive immune cell traffic to the penumbra region of rat's ischemic stroke brain.Iranian journal of basic medical sciences · 2025Article
- Nobiletin restores HFD-induced enteric nerve injury by regulating enteric glial activation and the GDNF/AKT/FOXO3a/P21 pathway.Molecular medicine (Cambridge, Mass.) · 2024Article
- Effect of Cyclosporin H on ischemic injury and neutrophil infiltration in cerebral infarct model of rats via PET imaging.Annals of nuclear medicine · 2024Article
- TREM2-IGF1 Mediated Glucometabolic Enhancement Underlies Microglial Neuroprotective Properties During Ischemic Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- sTREM2 in the prognostic evaluation of acute lung injury after cardiac surgery in infants.Pediatric research · 2024Article
- PA2G4/EBP1 ubiquitination by PRKN/PARKIN promotes mitophagy protecting neuron death in cerebral ischemia.Autophagy · 2024Article
23 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
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although post-ischemic inflammation induced by the innate immune response is considered an essential step in the progression of cerebral ischemia injury, the role of triggering receptor expressed on myeloid cells 2 (TREM2) in the pathogenesis of ischemic stroke remains to be elucidated. Here, we found that the transcriptional and post-transcriptional levels of TREM2 were increased in cultured primary microglia after oxygen-glucose deprivation and reoxygenation and in the ischemic penumbra of the cerebral cortex after middle cerebral artery occlusion (MCAO) and reperfusion in mice. TREM2 was mainly expressed in microglia, but not in astrocytes, neurons, or oligodendrocytes in mice subjected to MCAO. Manipulating TREM2 expression levels in vitro and in vivo significantly regulated the production of pro- and anti-inflammatory mediators after ischemic stroke. TREM2 overexpression markedly suppressed the inflammatory response and neuronal apoptosis. By contrast, TREM2 gene silencing intensified the inflammatory response, increased neuronal apoptosis and infarct volume, and further exacerbated neurological dysfunction. Our study demonstrated that TREM2 protects against cerebral ischemia/reperfusion injury through the aspect of post-ischemic inflammatory response and neuronal apoptosis. Pharmacological targeting of TREM2 to suppress the inflammatory response may provide a new approach for developing therapeutic strategies in the treatment of ischemic stroke and other cerebrovascular diseases.
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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.