Evidence map›Paper›PMID 27699598›Full record

ArticleMolecular neurobiology2017

Ischemic Post-Conditioning Induces Post-Stroke Neuroprotection via Hsp70-Mediated Proteasome Inhibition and Facilitates Neural Progenitor Cell Transplantation.

Thorsten R Doeppner, Maria Doehring, Britta Kaltwasser, Arshad Majid, Fengyan Lin, Mathias Bähr, Ertugrul Kilic, Dirk M Hermann

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 20% 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.

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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Neuroprotectants: The Next Frontier in Neurology.Journal of pharmacy & bioallied sciences · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Association betweenGenes · 2023
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

8 authors at 5 institutions in 4 countries.

Thorsten R DoeppnerDepartment of Neurology, University of Duisburg-Essen Medical School, Essen, Germany. thorsten.doeppner@uk-essen.de.
Maria DoehringOberhavel Kliniken, Department of Internal Medicine, Oranienburg, Germany.
Britta KaltwasserDepartment of Neurology, University of Duisburg-Essen Medical School, Essen, Germany.
Arshad MajidSheffield Institute for Translational Neuroscience, University of Sheffield, Sheffield, UK.
Fengyan LinCancer Center, The First Affiliated Hospital, Jilin University, Changchun, Jilin, China.
Mathias BährDepartment of Neurology, University of Göttingen Medical School, Göttingen, Germany.
Ertugrul KilicRegenerative and Restorative Medical Research Center, Istanbul Medipol University, Istanbul, Turkey.
Dirk M HermannDepartment of Neurology, University of Duisburg-Essen Medical School, Essen, Germany.
University of Duisburg-Essen · DEFirst Hospital of Jilin University · CNIstanbul Medipol University · TRUniversity of Göttingen · DEUniversity of Sheffield · GB

Funding

Tubitak 2221
6 · The paper itself

Abstract

In view of the failure of pharmacological therapies, alternative strategies promoting post-stroke brain repair are needed. Post-conditioning is a potentially promising therapeutic strategy, which induces acute neuroprotection against ischemic injury. To elucidate longer lasting actions of ischemic post-conditioning, mice were exposed to a 60-min stroke and post-conditioning by an additional 10-min stroke that was induced 10 min after reperfusion onset. Animals were sacrificed 24 h or 28 days post-stroke. Post-conditioning reduced infarct volume and neurological deficits 24 h post-stroke, enhancing blood-brain barrier integrity, reducing brain leukocyte infiltration, and reducing oxidative stress. On the molecular level, post-conditioning yielded increased Hsp70 expression, whereas nuclear factor (NF)-κB and proteasome activities were decreased. Reduced infarct volume and proteasome inhibition were reversed by Hsp70 knockdown, suggesting a critical role of the Hsp70 proteasome pathway in ischemic post-conditioning. The survival-promoting effects of ischemic post-conditioning, however, were not sustainable as neuroprotection and neurological recovery were lost 28 days post-stroke. Although angioneurogenesis was not increased by post-conditioning, the favorable extracellular milieu facilitated intracerebral transplantation of neural progenitor cells 6 h post-stroke, resulting in persisted neuroprotection and neurological recovery. Thus, post-conditioning might support brain repair processes, but in view of its transient, neuroprotection is unlikely useful as stroke therapy in its current form.

Indexed as

Ischemic PostconditioningStem Cell TransplantationAnimalsBrainDisease Models, AnimalHSP70 Heat-Shock ProteinsMaleMatrix Metalloproteinase 9MiceMice, Inbred C57BLNeural Stem CellsNeuroprotectionNF-kappa BOxidative StressProteasome Endopeptidase ComplexRecovery of FunctionHSP70 Heat-Shock ProteinsMatrix Metalloproteinase 9Mmp9 protein, mouseNF-kappa BProteasome Endopeptidase ComplexCerebral ischemiaHsp70Neural progenitor cellsPost-conditioningPreconditioningProteasomeStrokeTransplantation

Identifiers

PMID27699598
OpenAlexW2525949321

What OpenQuestion holds

Textmetadata
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.