Evidence map›Paper›PMID 29027964›Full record

ReviewInternational journal of molecular sciences2017

Microglia and Monocytes/Macrophages Polarization Reveal Novel Therapeutic Mechanism against Stroke.

Masato Kanazawa, Itaru Ninomiya, Masahiro Hatakeyama, Tetsuya Takahashi, Takayoshi Shimohata

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04088630 (Fingolimod as a Treatment of Cerebral Edema After Intracerebral Hemorrhage), which is not on this map. Cited by 224 papers.

0numbers the graph read from it
0cells of the map it votes in
224citing papers in PubMed
16.6field-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.

NCT04088630 early_phase1completednot on this mapstarted 2020, after this paper: background citation

Fingolimod as a Treatment of Cerebral Edema After Intracerebral Hemorrhage

TypeinterventionalSponsorWake Forest University Health SciencesRan2020 to 2024Enrolled28ConditionsIntracerebral Hemorrhage, Cerebral Edema, Stroke Hemorrhagic, Intracerebral Hemorrhage, HypertensiveArmsFingolimod, Placebo, Open-label Fingolimod
3 · Its place in the literature

Who cites it

224 citing papers in PubMed, 402 citations in OpenAlex.

  1. Article
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  4. Review
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164 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

5 authors at 3 institutions in 1 country.

Masato KanazawaDepartment of Neurology, Brain Research Institute, Niigata University, Niigata 951-8585, Japan. masa2@bri.niigata-u.ac.jp.ORCID 0000-0001-6337-8156
Itaru NinomiyaDepartment of Neurology, Brain Research Institute, Niigata University, Niigata 951-8585, Japan. ininomiya@bri.niigata-u.ac.jp.
Masahiro HatakeyamaDepartment of Neurology, Brain Research Institute, Niigata University, Niigata 951-8585, Japan. hatakeyama.mas@gmail.com.
Tetsuya TakahashiDepartment of Neurology, Niishi-Niigata Chuo Hospital, Niigata 950-2085, Japan. ttetsuya.neurology@gmail.com.
Takayoshi ShimohataDepartment of Neurology and Geriatrics, Gifu University Graduate School of Medicine, Gifu 501-1193, Japan. shimo@gifu-u.ac.jp.
Niigata University · JPGifu University · JPNishi Niigata Chuo National Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke is a leading cause of morbidity and mortality worldwide, and consists of two types, ischemic and hemorrhagic. Currently, there is no effective treatment to increase the survival rate or improve the quality of life after ischemic and hemorrhagic stroke in the subacute to chronic phases. Therefore, it is necessary to establish therapeutic strategies to facilitate functional recovery in patients with stroke during both phases. Cell-based therapies, using microglia and monocytes/macrophages preconditioned by optimal stimuli and/or any therapies targeting these cells, might be an ideal therapeutic strategy for managing stroke. Microglia and monocytes/macrophages polarize to the classic pro-inflammatory type (M1-like) or alternative protective type (M2-like) by optimal condition. Cell-based therapies using M2-like microglia and monocytes/macrophages might be protective therapeutic strategies against stroke for three reasons. First, M2-like microglia and monocytes/monocytes secrete protective remodeling factors, thus prompting neuronal network recovery via tissue (including neuronal) and vascular remodeling. Second, these cells could migrate to the injured hemisphere through the blood-brain barrier or choroid-plexus. Third, these cells could mitigate the extent of inflammation-induced injuries by suitable timing of therapeutic intervention. Although future translational studies are required, M2-like microglia and monocytes/macrophages therapies are attractive for managing stroke based on their protective functions.

Indexed as

Age FactorsAnimalsBiomarkersCell- and Tissue-Based TherapyCytokinesHumansMacrophage ActivationMacrophagesMicrogliaMonocytesPhenotypeSex FactorsStrokeTreatment OutcomeVascular RemodelingBiomarkersCytokinesM2-likemacrophagemicrogliamonocytepleiotropic effectspolarizationprotectivestroke

Identifiers

PMID29027964
PMCPMC5666817
OpenAlexW2761635843

What OpenQuestion holds

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LicenceCC BY
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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.