Evidence map›Paper›PMID 25475659›Full record

ReviewCNS neuroscience & therapeutics2015

Mechanisms and potential therapeutic applications of microglial activation after brain injury.

Jong-Youl Kim, Nuri Kim, Midori A Yenari

Abstract readReview
In one paragraph

Review in CNS neuroscience & therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing 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

71 citing papers in PubMed.

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  17. Agmatine-IRF2BP2 interaction induces M2 phenotype of microglia by increasing IRF2-KLF4 signaling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
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11 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.

Jong-Youl KimDepartment of Neurology, San Francisco Veterans Affairs Medical Center, University of California, San Francisco, San Francisco, CA, USA.
Nuri Kim
Midori A Yenari

Funding

Inflammatory Mechanisms in Cerebral IschemiaR01NS040516 · NINDS · STANFORD UNIVERSITY · PI YENARI, MIDORI A · 2001 to 2014
$4.6M
BLRD VA I01 BX000589NINDS NIH HHS NS40516NINDS NIH HHS R01 NS040516
6 · The paper itself

Abstract

As the resident immune cells of the central nervous system, microglia rapidly respond to brain insults, including stroke and traumatic brain injury. Microglial activation plays a major role in neuronal cell damage and death by releasing a variety of inflammatory and neurotoxic mediators. Their activation is an early response that may exacerbate brain injury and many other stressors, especially in the acute stages, but are also essential to brain recovery and repair. The full range of microglial activities is still not completely understood, but there is accumulating knowledge about their role following brain injury. We review recent progress related to the deleterious and beneficial effects of microglia in the setting of acute neurological insults and the current literature surrounding pharmacological interventions for intervention.

Indexed as

AnimalsBrain InjuriesBrain IschemiaHumansMicrogliaBrain injuryInflammationMicrogliaNeurotoxic mediator

Identifiers

PMID25475659
PMCPMC4376565

What OpenQuestion holds

Textmetadata
LicenceTDM
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.