ReviewMolecular neurobiology2026
The NETs-cGAS-STING Axis in Ischemic Stroke: Linking Neutrophil-Microglia Crosstalk, Immunothrombosis, and Neuroinflammation.
Review in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immune and inflammatory responses following ischemic stroke involve aberrant DNA exposure, immunothrombosis, and innate immune activation. Post-stroke, damage-associated DNA signals from multiple sources may activate DNA-sensing pathways; however, how DNA from distinct sources links peripheral immune activation with inflammatory amplification within the brain remains incompletely understood. Among these, neutrophil extracellular traps (NETs), as DNA-rich extracellular structures, may represent a potential link connecting vascular inflammation, immunothrombosis, and intracerebral DNA sensing. The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway, a key DNA-sensing axis, mediates distinct inflammatory and stress responses across various stroke-associated cell types. This review summarizes the mechanisms of DNA recognition, NET-mediated immunothrombosis, and neuroinflammatory damage, as well as the functional characteristics of cGAS-STING signaling in different cell types. Based on current evidence, we propose a potential NETs-cGAS-STING inflammatory amplification framework: NET-derived DNA may contribute to DNA-sensing activation within the ischemic brain and promote microglial inflammatory responses, while the resulting inflammatory factors and chemotactic signals may further promote neutrophil recruitment and secondary NET formation, thereby potentially creating a feed-forward loop linking peripheral immune activation with neuroinflammation. We further discuss the spatiotemporal heterogeneity of this axis, therapeutic targets, and challenges for clinical translation. Overall, the NETs-cGAS-STING framework provides an integrated conceptual perspective for understanding the intercellular interactions underlying DNA recognition and the sustained amplification of inflammation following stroke, and offers insights into future precision immune interventions tailored to disease stage, lesion characteristics, and cell-specific responses.
Indexed as
Identifiers
42570050What Socratic 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 Socratic graph.