ReviewNeurocritical care2021
Role of Interleukin-1 Receptor-Like 1 (ST2) in Cerebrovascular Disease.
Review in Neurocritical care, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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
7 citing papers in PubMed, 12 citations in OpenAlex.
- Brain Endothelial Soluble ST2 Production and Cerebral Edema in a Rat Model of Ischemic Stroke.Annals of neurology · 2026Article
- Associations of Soluble Serum Stimulation-2 With Functional Outcomes and Death at 1 Year in Acute Ischemic Stroke: A Prospective Cohort Study.Journal of the American Heart Association · 2025Observational
- Expanding Role of Interleukin-1 Family Cytokines in Acute Ischemic Stroke.International journal of molecular sciences · 2024Review
- Releasing Dynamic of Serum ST2 and Calprotectin in Patients with Acute Ischemic Stroke.Diagnostics (Basel, Switzerland) · 2024Article
- Association of Soluble ST2 With Functional Outcome, Perihematomal Edema, and Immune Response After Intraparenchymal Hemorrhage.Neurology · 2023Article
- The Prognostic Role of ST2L and sST2 in Patients Who Underwent Carotid Plaque Endarterectomy: A Five-Year Follow-Up Study.Journal of clinical medicine · 2022Article
- Neuroinflammation, Stem Cells, and Stroke.Stroke · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Following both ischemic and hemorrhagic stroke, innate immune cells initiate a proinflammatory response that further exacerbate tissue injury in the acute phase, but these cells also play an important reparative role thereafter. Numerous cytokines and signaling pathways have been implicated in driving the deleterious proinflammatory response, but less is known about the mediators that connect the initial vascular injury to the systemic immune response and the relationship between proinflammatory and reparative immune responses. The Interleukin-33 (IL-33) and serum stimulation-2 (ST2) axis is an interleukin signaling pathway that is a prime candidate to fulfill this role. In this review, we describe the biology of the IL-33/ST2 system, present evidence that its soluble decoy receptor, soluble ST2 (sST2), plays a key role in secondary neurologic injury after stroke, and discuss this in the context of the known role of IL-33/ST2 in other disease.
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.