ArticleInflammation2026
cGAMP Enhances Microglial/Macrophage Phagocytosis in Ischemic Stroke Via Activation of the TREM2-DAP10-PI3K Pathway.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- The CEBPB-AP-1 (JunB/Fos) Axis Drives Neuroinflammation and Microglial Dysfunction Via TNF Signaling in Ischemic Stroke.Inflammation · 2026Article
- Mitochondrial DNA as a driver of inflammation via the cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Ischemic stroke (IS), a multifaceted neurodegenerative disorder characterized by neuroinflammation and neuronal damage, is critically linked to the cGAS-STING pathway, a key mediator of neuroinflammatory responses during cerebral ischemia. However, the specific role of the STING agonist 2',3'-cGAMP (cGAMP) in modulating ischemic brain injury remains poorly understood. In this study, we investigated the therapeutic effects of cGAMP in a rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) and in BV2 microglial cells subjected to oxygen-glucose deprivation/reperfusion (OGD/R). Network pharmacology analysis was further employed to predict potential molecular targets and mechanisms underlying cGAMP's action in IS. To validate these findings, TREM2-specific small interfering RNA (siRNA) was utilized to suppress TREM2 expression, enabling mechanistic exploration of cGAMP's activity. Our results demonstrate that cGAMP exerts neuroprotective effects in IS through a noncanonical STING signaling pathway. Specifically, we reveal that cGAMP enhances microglial/macrophage phagocytic function via TREM2-dependent mechanisms. These findings provide novel insights into the therapeutic potential of cGAMP in IS and identify TREM2 as a promising target for modulating neuroinflammation and neuronal recovery in ischemic stroke.
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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 Socratic graph.