ArticleFrontiers in neuroscience2026
A NET-competent neutrophil subpopulation drives early brain injury after subarachnoid hemorrhage.
Article in Frontiers in neuroscience, 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
Introduction: Early brain injury (EBI) following subarachnoid hemorrhage (SAH) critically determines neurological outcomes, yet the cellular drivers remain unclear. Methods: To systematically dissect acute pathogenic programs, we performed single-cell RNAsequencing of CD45 Results: This revealed a 24-h-specific injury module enriched for inflammatory and myeloid-related pathways. Mapping this module onto the single-cell landscape identified neutrophils as the principal cellular mediators. High-resolution subclustering further defined a distinct neutrophil subset, N_04, as the primary carrier of the 24-h pathogenic signature. N_04 is transcriptionally primed for Neutrophil Extracellular Trap (NET) formation, with key effectors including Padi4, Mmp8, and Lcn2, and spatial mapping localized N_04 to regions adjacent to the puncture site. Transcriptional regulatory analysis identified Padi4, Nfe2, and Cebpe as central nodes sustaining N_04 effector identity, while Discussion: Collectively, these findings define a NET-competent neutrophil subpopulation as a central driver of acute post-SAH brain injury and nominate Padi4-dependent NETosis as a potential therapeutic target.
Indexed as
Identifiers
What 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.