Evidence map›Paper›PMID 30483945›Full record

ReviewActa neuropathologica2019

Post-stroke inflammation-target or tool for therapy?

Kate Lykke Lambertsen, Bente Finsen, Bettina Hjelm Clausen

Registry-linked trialOpen access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Acta neuropathologica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07754942 (Local-to-Systemic Inflammatory Biomarker Gradients and 90-Day Functional Outcomes in Patients With Acute Ischemic Stroke Due to Anterior Circulation Large Vessel Occlusion Undergoing Mechanical Thrombectomy), which is not on this map. Cited by 282 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
282citing papers in PubMed, 6 pooled it
15.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

NCT07754942 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Local-to-Systemic Inflammatory Biomarker Gradients and 90-Day Functional Outcomes in Patients With Acute Ischemic Stroke Due to Anterior Circulation Large Vessel Occlusion Undergoing Mechanical Thrombectomy: A Prospective Observational Cohort Study

TypeobservationalSponsorZhongshan Hospital Xiamen UniversityRan2026 to 2029Enrolled50ConditionsAcute Ischemic Stroke, Large Vessel OcclusionArmsProspective Mechanical Thrombectomy Cohort
3 · Its place in the literature

Who cites it

282 citing papers in PubMed, 6 syntheses or guidelines pooled it, 455 citations in OpenAlex.

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222 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Kate Lykke LambertsenDepartment of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, 5000, Odense, Denmark. klambertsen@health.sdu.dk.ORCID 0000-0001-9276-4902
Bente FinsenDepartment of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, 5000, Odense, Denmark.
Bettina Hjelm ClausenDepartment of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, 5000, Odense, Denmark.
University of Southern Denmark · DK

Funding

Lundbeckfonden R126-A11512Lundbeckfonden R173-2014-955Lundbeckfonden R54-A5539Lundbeckfonden R67-A6383Novo Nordisk Fonden NNF12OC0002215Sundhed og Sygdom, Det Frie Forskningsråd DFF-4183-00033
6 · The paper itself

Abstract

Inflammation is currently considered a prime target for the development of new stroke therapies. In the acute phase of ischemic stroke, microglia are activated and then circulating immune cells invade the peri-infarct and infarct core. Resident and infiltrating cells together orchestrate the post-stroke inflammatory response, communicating with each other and the ischemic neurons, through soluble and membrane-bound signaling molecules, including cytokines. Inflammation can be both detrimental and beneficial at particular stages after a stroke. While it can contribute to expansion of the infarct, it is also responsible for infarct resolution, and influences remodeling and repair. Several pre-clinical and clinical proof-of-concept studies have suggested the effectiveness of pharmacological interventions that target inflammation post-stroke. Experimental evidence shows that targeting certain inflammatory cytokines, such as tumor necrosis factor, interleukin (IL)-1, IL-6, and IL-10, holds promise. However, as these cytokines possess non-redundant protective and immunoregulatory functions, their neutralization or augmentation carries a risk of unwanted side effects, and clinical translation is, therefore, challenging. This review summarizes the cell biology of the post-stroke inflammatory response and discusses pharmacological interventions targeting inflammation in the acute phase after a stroke that may be used alone or in combination with recanalization therapies. Development of next-generation immune therapies should ideally aim at selectively neutralizing pathogenic immune signaling, enhancing tissue preservation, promoting neurological recovery and leaving normal function intact.

Indexed as

AnimalsBrain IschemiaCytokinesDisease Models, AnimalHumansInflammationMicrogliaStrokeCytokinesCytokinesDrugsImmune therapyIschemiaNeuroprotection

Identifiers

PMID30483945
PMCPMC6482288
OpenAlexW2900430109

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.