Evidence map›Paper›PMID 41062473›Full record

ArticleNature communications2025

Exercise facilitates post-stroke recovery through mitigation of neuronal hyperexcitability via interleukin-10 signaling.

A Schmidt-Pogoda, T Ruck, J K Strecker, M Hoppen, L Fazio, L Vinnenberg, B Maus, L Wachsmuth, M Cerina, K Diederich and 21 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Brain-muscle axis regulation of neuroinflammation and sarcopenia in Parkinson's disease: the bridging role of lactylation.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Insights gained from single-cell sequencing analysis of ischemic stroke.Frontiers in cell and developmental biology · 2026
    Review
  7. Review
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

31 authors.

A Schmidt-PogodaDepartment of Neurology, University of Münster, Münster, Germany. antje.schmidt-pogoda@ukmuenster.de.
T RuckDepartment of Neurology, Ruhr University Bochum, BG University Hospital Bergmannsheil, Bochum, Germany.ORCID http://orcid.org/0000-0001-6332-8650
J K StreckerDepartment of Neurology, University of Münster, Münster, Germany.
M HoppenDepartment of Neurology, University of Münster, Münster, Germany.
L FazioDepartment of Neurology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
L VinnenbergDepartment of Neurology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.ORCID http://orcid.org/0000-0001-8843-007X
B MausClinic of Radiology, University of Münster, Münster, Germany.ORCID http://orcid.org/0000-0003-1872-9097
L WachsmuthClinic of Radiology, University of Münster, Münster, Germany.
M CerinaDepartment of Neurology, University of Münster, Münster, Germany.
K DiederichDepartment of Neurology, University of Münster, Münster, Germany.
S LichtenbergDepartment of Neurology, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.ORCID http://orcid.org/0000-0003-4703-2571
H AbbergerInstitute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0001-8192-7761
Lal HaertelDepartment of Neurology, University of Münster, Münster, Germany.
D SchafflickDepartment of Neurology, University of Münster, Münster, Germany.ORCID http://orcid.org/0000-0001-5908-4745
G Meyer Zu HörsteDepartment of Neurology, University of Münster, Münster, Germany.ORCID http://orcid.org/0000-0002-4341-4719
A M HerrmannDepartment of Neurology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
P HundehegeDepartment of Neurology, University of Münster, Münster, Germany.
V NarayananDepartment of Neurology, University of Münster, Münster, Germany.
C NelkeDepartment of Neurology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.
K KruithoffDepartment of Neurology, University of Münster, Münster, Germany.
J BosbachDepartment of Neurology, University of Münster, Münster, Germany.
E VicariDepartment of Dermatology, Heidelberg University Hospital, Heidelberg, Germany.
T RamckeDepartment of Dermatology, Heidelberg University Hospital, Heidelberg, Germany.
C BeukerDepartment of Neurology, University of Münster, Münster, Germany.
E HadaschikDepartment of Dermatology, Heidelberg University Hospital, Heidelberg, Germany.
T BuddeInstitute of Physiology I, University of Münster, Münster, Germany.ORCID http://orcid.org/0000-0002-5263-8183
C FaberClinic of Radiology, University of Münster, Münster, Germany.ORCID http://orcid.org/0000-0001-7683-7710
H WiendlDepartment of Neurology, University of Münster, Münster, Germany.ORCID http://orcid.org/0000-0003-4310-3432
W HansenInstitute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
S G MeuthDepartment of Neurology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.ORCID http://orcid.org/0000-0003-2571-3501
J MinnerupDepartment of Neurology, University of Münster, Münster, Germany. minnerup@uni-muenster.de.

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) GRK2515Massachusetts Department of Fish and Game (DFG) BD604920
6 · The paper itself

Abstract

Physical exercise is an effective therapy for improving stroke recovery. However, the exact underlying molecular mechanisms of exercise-enhanced neuronal repair remain unclear. As exercise affects the immune system in healthy individuals, and the immune system in turn influences recovery after stroke, we hypothesized that immune mechanisms play a role in exercise-induced neurological recovery. Using a model of ischemic stroke in adult male mice, we here show that the presence of regulatory T cells (Treg) within the ischemic brain is a prerequisite for exercise-enhanced functional and structural recovery. Treg prevent excessive and sustained hyperexcitability of periinfarct neurons via IL-10 signaling. This reduced hyperexcitability precedes alterations in neuronal connectivity, which underlie functional improvement. Together, we delineate the interaction of exercise-therapy, the immune system and functional recovery after ischemic stroke. Our findings can have translational relevance for further development of immune-targeted therapies.

Indexed as

Interleukin-10Ischemic StrokeNeuronsPhysical Conditioning, AnimalStrokeStroke RehabilitationAnimalsBrainBrain IschemiaDisease Models, AnimalMaleMiceMice, Inbred C57BLRecovery of FunctionSignal TransductionT-Lymphocytes, RegulatoryIL10 protein, mouseInterleukin-10

Identifiers

PMID41062473
PMCPMC12508215

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Registered trials

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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.