Evidence map›Paper›PMID 38872149›Full record

ArticleJournal of neuroinflammation2024

Delayed plasma kallikrein inhibition fosters post-stroke recovery by reducing thrombo-inflammation.

Steffen Haupeltshofer, Stine Mencl, Rebecca D Szepanowski, Christina Hansmann, Ana I Casas, Hanna Abberger, Wiebke Hansen, Alina Blusch, Cornelius Deuschl, Michael Forsting and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. The kallikrein-kinin system modulates CD4Journal of neuroinflammation · 2026
    Article
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

13 authors.

Steffen HaupeltshoferDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Hospital Essen, Hufelandstr. 55, D-45147, Essen, Germany. steffen.haupeltshofer@uk-essen.de.
Stine MenclDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Hospital Essen, Hufelandstr. 55, D-45147, Essen, Germany.
Rebecca D SzepanowskiDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Hospital Essen, Hufelandstr. 55, D-45147, Essen, Germany.
Christina HansmannDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Hospital Essen, Hufelandstr. 55, D-45147, Essen, Germany.
Ana I CasasDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Hospital Essen, Hufelandstr. 55, D-45147, Essen, Germany.
Hanna AbbergerInstitute of Medical Microbiology, University Hospital Essen, Virchowstr. 179, D-45147, Essen, Germany.
Wiebke HansenInstitute of Medical Microbiology, University Hospital Essen, Virchowstr. 179, D-45147, Essen, Germany.
Alina BluschDepartment of Neurology, Center for Huntington's Disease NRW, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstr. 56, D-44791, Bochum, Germany.
Cornelius DeuschlInstitute of Diagnostic and Interventional Radiology and Neuroradiology, University Hospital Essen, Hufelandstr. 55, D-45147, Essen, Germany.
Michael ForstingInstitute of Diagnostic and Interventional Radiology and Neuroradiology, University Hospital Essen, Hufelandstr. 55, D-45147, Essen, Germany.
Dirk M HermannDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Hospital Essen, Hufelandstr. 55, D-45147, Essen, Germany.
Friederike Langhauser *Department of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Hospital Essen, Hufelandstr. 55, D-45147, Essen, Germany.
Christoph Kleinschnitz *Department of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Hospital Essen, Hufelandstr. 55, D-45147, Essen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of the kallikrein-kinin system promotes vascular leakage, inflammation, and neurodegeneration in ischemic stroke. Inhibition of plasma kallikrein (PK) - a key component of the KKS - in the acute phase of ischemic stroke has been reported to reduce thrombosis, inflammation, and damage to the blood-brain barrier. However, the role of PK during the recovery phase after cerebral ischemia is unknown. To this end, we evaluated the effect of subacute PK inhibition starting from day 3 on the recovery process after transient middle artery occlusion (tMCAO). Our study demonstrated a protective effect of PK inhibition by reducing infarct volume and improving functional outcome at day 7 after tMCAO. In addition, we observed reduced thrombus formation in cerebral microvessels, fewer infiltrated immune cells, and an improvement in blood-brain barrier integrity. This protective effect was facilitated by promoting tight junction reintegration, reducing detrimental matrix metalloproteinases, and upregulating regenerative angiogenic markers. Our findings suggest that PK inhibition in the subacute phase might be a promising approach to accelerate the post-stroke recovery process.

Indexed as

Plasma KallikreinRecovery of FunctionAnimalsBlood-Brain BarrierInfarction, Middle Cerebral ArteryInflammationIschemic StrokeMaleMiceMice, Inbred C57BLStrokeThrombosisPlasma KallikreinBlood-brain barrierExtravasationInflammationIschemic strokeKallikrein-kinin systemPlasma kallikreinRecoverySubacuteThrombo-inflammationThrombosis

Identifiers

PMID38872149
PMCPMC11177352

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.