ArticleAnnals of neurology2026
Brain Endothelial Soluble ST2 Production and Cerebral Edema in a Rat Model of Ischemic Stroke.
Article in Annals of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- A roadmap towards clinical use of molecular biomarkers in acute ischaemic stroke.Nature reviews. Neurology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
objectiveNo current therapy prevents swelling after ischemic stroke, and pathways leading to edema formation are not completely understood. We have found the immune regulator soluble ST2 (sST2) to be a candidate mediator of edema formation. In the current study, we sought to identify a mechanistic relationship between sST2 and edema in ischemic stroke.
methodsWe conducted a proteomics survey for plasma biomarkers of edema in patients with large ischemic stroke and verified associations with outcome. We performed middle-cerebral artery occlusion (MCAO) in rats and measured sST2 expression. We used both in vitro and in vivo techniques to determine the cellular source of sST2. We generated a sST2 knockout rat line and performed MCAO to determine the effect of knockout on brain edema, endothelial and microglial gene expression, and blood-brain barrier integrity.
resultsWe found sST2 to be associated with edema, outcome and mortality after large ischemic stroke. We replicated the elevation in plasma sST2 in a rat model of stroke and found brain endothelium as the cell type with highest expression. Knockout of sST2 did not alter lesion volume but was associated with reduced swelling and increased staining for the tight junction protein zona occludens 1 (ZO-1).
interpretationPlasma sST2 level is associated with edema, functional outcome, and mortality after ischemic stroke. Knockout of sST2 reduced post-stroke cerebral edema and was associated with increased staining for the tight junction protein ZO-1. These findings establish a mechanistic link between sST2 and brain edema and highlight its potential as a future therapeutic target. ANN NEUROL 2026;99:134-147.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.